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Anti-VEGF therapy in the management of retinopathy of prematurity: what we learn from representative animal models of oxygen-induced retinopathy
Dergi Makalesi

Dergi Makalesi
Open Access
Kaynak :
Directory of Open Access Journals (DOAJ)
Dergi:
Eye and Brain
Yazar(lar) :
Wang H
Yıl :
2016
Wang H
Yayıncı Web Sitesi
Kaydet Alıntıla
Haibo Wang Department of Ophthalmology, John A Moran Eye Center, The University of Utah, Salt Lake City, UT, USA Abstract: Retinopathy of prematurity (ROP) remains a leading cause of childhood blindness, affecting infants born prematurely. ROP is characterized by the onset of delayed physiological retinal vascular development (PRVD) and followed by pathologic neovascularization into the vitreous instead of the retina, called intravitreal neovascularization (IVNV). Therefore, the therapeutic strategy for treating ROP is to promote PRVD and inhibit or prevent IVNV. Vascular endothelial growth factor (VEGF) plays an important role in the pathogenesis of ROP. There is a growing body of studies testing the use of anti-VEGF agents as a treatment for ROP. Intravitreal anti-VEGF treatment for ROP has potential advantages compared with laser photocoagulation, the gold standard for the treatment of severe ROP; however, intravitreal anti-VEGF treatment has been associated with reactivation of ROP and suppression of systemic VEGF that may affect body growth and organ development in preterm infants. Therefore, it is important to understand the role of VEGF in PRVD and IVNV. This review includes the current knowledge of anti-VEGF treatment for ROP from animal models of oxygen-induced retinopathy (OIR), highlighting the importance of VEGF inhibition by targeting retinal Müller cells, which inhibits IVNV and permits PRVD. The signaling events involved in mediating VEGF expression and promoting VEGF-mediated angiogenesis, including hypoxia-dependent signaling, erythropoietin/erythropoietin receptor-, oxidative stress-, beta-adrenergic receptor-, integrin-, Notch/Delta-like ligand 4- and exon guidance molecules-mediated signaling pathways, are also discussed. Keywords: vascular endothelial growth factor, retinopathy of prematurity, intravitreal neovascularization, oxygen-induced retinopathy model, physiological retinal vascular development
Anahtar Kelimeler : Vascular endothelial growth factor, Retinopathy of prematurity, Intravitreal neovascularization, Oxygen induced retinopathy model, Physiological Retinal vascular development
ISSN: 1179-2744
Cilt: 2016
Sayı: 1
Sayfa: 81 - 90
Sınıflandırma :
2
Development and Preliminary Application of an Indirect ELISA to Detect Infectious Bovine Rhinotracheitis Virus Using Recombinant Glycoprotein D of IBRV Strain SD
Dergi Makalesi

Dergi Makalesi
Kaynak :
Sobiad Atıf Dizini
Dergi:
Kafkas Üniversitesi Veteriner Fakültesi Dergisi
Yazar(lar) :
SONG L , ZHANG H , WANG H , ZHAO G
WANG H
Yayıncı Web Sitesi
 Piri Tam Metin Bulucu
Kaydet Alıntıla
DOI : 10.9775/kvfd.2015.14890
3
IGFBP-3 Is the Key Target of Sanguinarine in Promoting Apoptosis in Hepatocellular Carcinoma
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Dergi Makalesi
Open Access
Kaynak :
Directory of Open Access Journals (DOAJ)
Dergi:
Cancer Management and Research
Yazar(lar) :
Wang H , Wang H , Li K , Li S , Sun B
Yıl :
2020
Wang H Wang H
Yayıncı Web Sitesi
Kaydet Alıntıla
Huiwen Wang,1,* He Wang,1,* Kai Li,1 Shijie Li,1 Bingyi Sun2 1Department of Interventional, Harbin Medical University Cancer Hospital, Harbin 150081, Heilongjiang Province, People’s Republic of China; 2Department of General Surgery, The First Hospital of Qiqihar, Qiqihar 161005, Heilongjiang Province, People’s Republic of China*These authors contributed equally to this workCorrespondence: Bingyi SunDepartment of General Surgery, The First Hospital of Qiqihar (Equals to: Affiliated Qiqihar Hospital, Southern Medical University), Qiqihar 161005, Heilongjiang Province, People’s Republic of ChinaEmail sunbingyi82@163.comIntroduction: Chemotherapeutic treatment of hepatocellular carcinoma (HCC) has always been plagued by nonspecific and side effects. Plant extracts have potential anticancer capabilities with low cytotoxicity and few side effects, but their detailed mechanisms are still unclear, thus limiting their clinical applications.Methods: In this study, five plant extracts were chosen, their inhibition on HCC cell viability was compared by CCK-8 assay and sanguinarine (SAN) was selected. Then, wound healing assay, transwell assay, and apoptosis assay were carried out in Hep3B cells. Bioinformatics methods were performed and IGFBP-3 was predicted the targets of SAN in HCC. The mechanism of SAN regulating IGFBP-3 was explored using qRT-PCR, Western blotting, cell viability assay and apoptosis assay. Meanwhile, knockdown of IGFBP-3 were used by small interfering RNA (siRNA).Results: In five plant extracts, SAN inhibited the proliferation of HCC cell lines most considerably. In addition, apoptosis was promoted, and invasion and migration were inhibited in the Hep3B cell line by treatment with SAN at 2 μM. Bioinformatics indicated that SAN could affect HCC apoptosis through the TP53/IGFBP-3 pathway, and further verification experiments showed that SAN upregulated the expression of insulin-like growth factor binding protein-3 (IGFBP-3) in the Hep3B cell line; SAN also inhibited the expression of Bcl-2 and promoted the expression of BAX and caspase-3. After using siRNA to inhibit the expression of IGFBP-3, the effect of SAN was blocked.Conclusion: Our study further reveals a novel mechanism that IGFBP-3 is an important target of SAN, by upregulating expression of IGFBP-3, SAN promotes apoptosis in HCC.Keywords: sanguinarine, IGFBP-3, apoptosis, hepatocellular carcinoma
Anahtar Kelimeler : sanguinarine, igfbp-3, apoptosis, hepatocellular carcinoma
ISSN: 1179-1322
Cilt: 12
Sayfa: 1007 - 1015
Sınıflandırma :
4
The influence of vascular endothelial growth factor-A and matrix metalloproteinase-2 and -9 in angiogenesis, metastasis, and prognosis of endometrial cancer
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Dergi Makalesi
Open Access
Kaynak :
Directory of Open Access Journals (DOAJ)
Dergi:
OncoTargets and Therapy
Yazar(lar) :
Mahecha AM , Wang H
Yıl :
2017
Wang H
Yayıncı Web Sitesi
Kaydet Alıntıla
Anna M Mahecha, Hongbo Wang Department of Obstetrics and Gynecology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China Abstract: Angiogenesis (the growth of new blood vessels) is essential in most of the body’s physiological processes, such as in the normal functioning of the endometrium during and after the menstrual cycle. Vascular endothelial growth factor (VEGF) and matrix metalloproteinase (MMP) are the mostly expressed angiogenic factors, especially, during the process of endometrial degeneration and remodeling. In carcinogenesis, tumor hypoxia-induced factors, through the process of “angiogenic switch”, stimulate the production of angiogenic factors, particularly VEGF and MMP. Subsequently, these angiogenic factors are associated with degradation, differentiation, proliferation, and migration of vascular endothelial cells, enhancing the formation of new blood vessels to supply the tumor with oxygen and nutrients. This process is equally significant for tumor development and metastasis. Hence, like in other cancers, the overexpression of MMP and VEGF in endometrial cancer (EC) seems to play a significant role in its tumorigenesis and metastasis. This research will discuss the influence of MMP and VEGF on angiogenesis, metastasis, and the prognosis of EC as well as the clinical importance of the factors in the diagnosis of EC. Keywords: angiogenic switch, angiogenic factors, endometrioid endometrial carcinoma, microvascular density
Anahtar Kelimeler : Angiogenic switch, angiogenic factors, endometrioid endometrial carcinoma, microvascular density.
ISSN: 1178-6930
Cilt: 10
Sayfa: 4617 - 4624
Sınıflandırma :
5
Epidemiology of Japanese encephalitis: past, present, and future prospects
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Dergi Makalesi
Open Access
Kaynak :
Directory of Open Access Journals (DOAJ)
Dergi:
Therapeutics and Clinical Risk Management
Yazar(lar) :
Wang H , Liang G
Yıl :
2015
Wang H
Yayıncı Web Sitesi
Kaydet Alıntıla
Huanyu Wang,1,2 Guodong Liang1,21State Key Laboratory for Infectious Disease Prevention and Control (SKLID), Department of Viral Encephalitis, Institute for Viral Disease Control and Prevention, Chinese Center for Disease Control and Prevention, Beijing People’s Republic of China; 2Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, Hangzhou, People’s Republic of China Abstract: Japanese encephalitis (JE) is one of severe viral encephalitis that affects individuals in Asia, western Pacific countries, and northern Australia. Although 67,900 JE cases have been estimated among 24 JE epidemic countries annually, only 10,426 have been reported in 2011. With the establishment of JE surveillance and vaccine use in some countries, the JE incidence rate has decreased; however, serious outbreaks still occur. Understanding JE epidemics and identifying the circulating JE virus genotypes will improve JE prevention and control. This review summarizes the current epidemiology data in these countries. Keywords: Japanese encephalitis, Japanese encephalitis virus, acute encephalitis syndrome
Cilt: 2015
Sayı: default
Sayfa: 435 - 448
Sınıflandırma :
Viroloji %97
6
The expression and significance of Gal-3 and MUC1 in colorectal cancer and colon cancer
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Dergi Makalesi
Open Access
Kaynak :
Directory of Open Access Journals (DOAJ)
Dergi:
OncoTargets and Therapy
Yazar(lar) :
Wang H , Wang L
Yıl :
2015
Wang H
Yayıncı Web Sitesi
Kaydet Alıntıla
Hong-shan Wang,1 Li-hong Wang2 1General Surgery Department, Zhengzhou People’s Hospital, Zhengzhou City, Henan Province, People’s Republic of China; 2Department of Gastroenterology, Zhengzhou Central Hospital of Zhengzhou University, Zhengzhou City, Henan Province, People’s Republic of China Objective: The objective of the present investigation was to explore the expression and significance of Gal-3 and MUC1 in colorectal cancer tissue and tissue adjacent to carcinoma.Methods: In this study we collected colorectal cancer tissues and the tissues adjacent to carcinoma from 45 cases from the Colorectal Cancer Surgery Department of Zhengzhou People’s Hospital from December of 2009 to June of 2010. At the same time, this study also collected nontumor tissues adjacent to carcinoma from 20 cases as the control group. The expression of Gal-3 and MUC1 of these tissues was detected by using immunohistochemistry streptavidin-peroxidase method, and the correlation between colorectal cancer and expression of Gal-3 and MUC1 was analyzed.Results: The positive expression rates of Gal-3 in the tissues adjacent to carcinoma and colorectal cancer were 15.0% and 73.3%, respectively. The positive expression rate of Gal-3 in colorectal cancer was significantly higher than that in the tissue adjacent to carcinoma. The positive expression rate of Gal-3 of the patients without lymph node metastasis was 61.5% (16/26). The positive expression rate of Gal-3 in the patients with lymph node metastasis was 89.5% (17/19), and the difference was statistically significant (P=0.0363). The positive expression rates of MUC1 in the tissues adjacent to carcinoma and in colorectal cancer tissues were 0.0% and 54.5%, respectively. The positive expression rate of MUC1 in colorectal cancer tissues was significantly higher than that in the normal tissues adjacent to carcinoma (P<0.05); the positive expression rate of MUC1 in the patients without lymph node metastasis was 34.6% (9/26). The positive expression rate of MUC1 in the patients with lymph node metastasis was 84.2% (16/19), and the expression difference was statistically significant (P=0.0009).Conclusion: The expression of Gal-3 and MUC1 was significantly higher than that in the nontumor tissue adjacent to carcinoma. There was a correlation between Gal-3 and MUC1 expression and lymphatic metastasis. Keywords: immunohistochemistry, lymph node metastasis, invasion of tumor
ISSN: 1178-6930
Cilt: 2015
Sayı: default
Sayfa: 1893 - 1898
Sınıflandırma :
7
An update on gene therapy for the treatment of lipoprotein lipase deficiency
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Dergi Makalesi
Open Access
Kaynak :
Directory of Open Access Journals (DOAJ)
Dergi:
Orphan Drugs: Research and Reviews
Yazar(lar) :
Libby AE , Wang H
Yıl :
2014
Wang H
Yayıncı Web Sitesi
Kaydet Alıntıla
Andrew E Libby, Hong Wang Division of Endocrinology, Metabolism, and Diabetes, School of Medicine, University of Colorado at Denver, Aurora, CO, USA Abstract: Lipoprotein lipase (LPL) is responsible for clearance of triglyceride-rich lipoproteins from the blood. Deficiency or defects in this enzyme result in profound hypertriglyceridemia and susceptibility to chronic, life-threatening pancreatitis. Management of LPL deficiency has traditionally been restricted to palliative care and strategies to reduce the risk of pancreatitis, including severe dietary restrictions of fat. Recently, the European Commission approved the first gene therapy treatment in the West to treat this rare disease. Alipogene tiparvovec (Glybera®) was granted marketing authorization in November 2012 to treat LPL deficiency in a subset of patients that are at increased risk for pancreatitis. Designed as a one-time treatment, the drug uses adeno-associated virus (AAV1) delivery of transgenic LPL to muscle in patients lacking functional enzyme. Although statistically significant reduction of serum triglycerides was initially observed in trial subjects, this effect was found to be transient, with triglyceride levels eventually rebounding to basal levels by 26 weeks in all participants. Nevertheless, despite the return of triglycerides to pretreatment levels, alipogene tiparvovec was found to have a long-term impact on postprandial chylomicron metabolism by lowering the fraction of triglyceride found in this subset of lipoproteins. Furthermore, the drug led to a clinically significant reduction in the incidence of pancreatitis in LPL-deficient patients. The regulatory approval of alipogene tiparvovec was a historic process and serves as an example of the challenges that future orphan drugs will face. Keywords: lipoprotein lipase deficiency, gene therapy, AAV, chylomicron, pancreatitis
Anahtar Kelimeler : lipoprotein lipase deficiency, gene therapy, chylomicron, pancreatitis
ISSN: 2230-6161
Cilt: 2014
Sayı: 1
Sayfa: 47 - 54
Sınıflandırma :
8
Evaluation of the Efficacy of Neoadjuvant Chemotherapy for Breast Cancer
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Dergi Makalesi
Open Access
Kaynak :
Directory of Open Access Journals (DOAJ)
Dergi:
Drug Design, Development and Therapy
Yazar(lar) :
Wang H , Mao X
Yıl :
2020
Wang H
Yayıncı Web Sitesi
Kaydet Alıntıla
Huan Wang, Xiaoyun Mao Department of Breast Surgery, The First Affiliated Hospital of China Medical University, Shenyang City, Liaoning Province, People’s Republic of ChinaCorrespondence: Xiaoyun MaoDepartment of Breast Surgery, The First Affiliated Hospital of China Medical University, 155 Nanjing North Street, Heping District, Shenyang City, Liaoning Province 110001, People’s Republic of ChinaTel/ Fax +86 24 83282618Email xymao@cmu.edu.cnAbstract: Neoadjuvant chemotherapy is increasingly used in breast cancer, especially for downstaging the primary tumor in the breast and the metastatic axillary lymph node. Accurate evaluations of the response to neoadjuvant chemotherapy provide important information on the impact of systemic therapies on breast cancer biology, prognosis, and guidance for further therapy. Moreover, pathologic complete response is a validated and valuable surrogate prognostic factor of survival after therapy. Evaluations of neoadjuvant chemotherapy response are very important in clinical work and basic research. In this review, we will elaborate on evaluations of the efficacy of neoadjuvant chemotherapy in breast cancer and provide a clinical evaluation procedure for neoadjuvant chemotherapy.Keywords: neoadjuvant chemotherapy, breast cancer, evaluations of response
Anahtar Kelimeler : neoadjuvant chemotherapy, breast cancer, evaluations of response
ISSN: 1177-8881
Cilt: 14
Sayfa: 2423 - 2433
Sınıflandırma :
9
Numerical limit analysis of the ultimate load bearing capacity of a pier foundation under complex load
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Dergi Makalesi
Open Access
Kaynak :
Directory of Open Access Journals (DOAJ)
Dergi:
MATEC Web of Conferences
Yazar(lar) :
Wang H F , Cheng X H
Yıl :
2019
Wang H F
Yayıncı Web Sitesi
Tam Metin
Kaydet Alıntıla
A pier foundation has plenty of advantages as the foundation form for large onshore wind turbines in the terrain of the Gobi desert and collapsible loess areas. The ultimate load bearing capacity design, as an important part in the design phase of this foundation form, is not sufficiently in terms of design theory and the checking method, especially for application in collapsible loess areas. In this paper, numerical limit analysis has been employed to analyze the load bearing capacity for the scheme of selection of a pier foundation of a 100 MW wind farm in certain collapsible loess geology in Ningxia. The results were then compared with the empirical formulas, the limit equilibrium solutions and the finite element solutions to verify the accuracy of the results. It has been demonstrated that under the ultimate engineering load, the pier foundation can meet the stability requirement. In the ultimate state, whether the surrounding soil of the foundation falls in plasticity is associated with the ratio of the depth to the diameter of the foundation. The numerical limit analysis method can automatically determine the failure surface.
DOI : 10.1051/matecconf/201927702018
ISSN: 2261-236X
Cilt: 277
Sayfa: 02018
Sınıflandırma :
10
Emerging options for the treatment of type 2 diabetes in Chinese patients: focus on arterial function and alogliptin
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Dergi Makalesi
Open Access
Kaynak :
Directory of Open Access Journals (DOAJ)
Dergi:
Drug Design, Development and Therapy
Yazar(lar) :
Wang H , Liu J , Zhao H
Yıl :
2015
Wang H
Yayıncı Web Sitesi
Kaydet Alıntıla
Hongyu Wang, Jinbo Liu, Hongwei Zhao Department of Vascular Medicine, Peking University Shougang Hospital, Beijing, People's Republic of China Abstract: Type 2 diabetes mellitus (T2DM) has become a worldwide health problem, and the rate of it is growing greatly in the People's Republic of China every year. T2DM could cause macrovascular and microvascular complications that lead to an increase in arterial wall thickness, endothelial dysfunction, calcification, and – finally – to an increase in arterial stiffness and arterial dysfunction. Alogliptin, a new selective inhibitor of dipeptidyl peptidase 4, has shown its great antihyperglycemia effect in T2DM patients. The clinical trial data from the People's Republic of China was similar to other global and Asian trials. This could provide some choice for clinical physicians to the treatment of T2DM. Keywords: type 2 diabetes mellitus, People's Republic of China, alogliptin, arterial function
ISSN: 1177-8881
Cilt: 2015
Sayı: default
Sayfa: 683 - 686
Sınıflandırma :
11
Circular RNA hsa_circ_0072309 inhibits proliferation and invasion of breast cancer cells via targeting miR-492
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Dergi Makalesi
Open Access
Kaynak :
Directory of Open Access Journals (DOAJ)
Dergi:
Cancer Management and Research
Yazar(lar) :
Yan L , Zheng M , Wang H
Yıl :
2019
Wang H
Yayıncı Web Sitesi
Kaydet Alıntıla
Lin Yan,1 Min Zheng,1 Hua Wang2 1Department of Breast Surgery, The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University, Wenzhou 325000, China; 2Department of Neurosurgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China Background: Although the number of circular RNAs (circRNAs) that has been identified in multiple cancer tissues continues to increase, the relationship between circRNA expression and carcinogenesis remains unknown. The role of hsa_circ_0072309 in breast cancer has remained undefined until now. In this study, we aimed to investigate the role of hsa_circ_0072309 in breast cancer progression. Methods: hsa_circ_0072309 expression in breast cancer tissues was analyzed using qRT-PCR. A series of functional experiments were carried out to investigate hsa_circ_0072309 function in breast cancer development and its underlying molecular mechanisms. Results: hsa_circ_0072309 expression in breast cancer tissues was upregulated relative to that in adjacent normal tissues. hsa_circ_0072309 could serve as a prognostic biomarker of breast cancer. hsa_circ_0072309 overexpression dramatically inhibited the proliferation, migration, and invasion of breast cancer cells in vitro. In vivo assays revealed that the ectopic expression of hsa_circ_0072309 repressed breast cancer growth. The results of our mechanistic studies indicated that hsa_circ_0072309 could act as the sponge of miR-492, which exhibited increased expression in breast cancer tissues. Hsa_circ_0072309 suppressed breast cancer cell proliferation, migration, and invasion by inhibiting miR-492. Conclusion: Our findings revealed for the first time that the hsa_circ_0072309-miR-492 axis plays an essential role in breast cancer progression. Keywords: circular RNA, hsa_circ_0072309, miR-492, breast cancer, progression
Anahtar Kelimeler : circular RNA, hsa_circ_0072309, miR-492, breast cancer, progression
ISSN: 1179-1322
Cilt: 11
Sayfa: 1033 - 1041
Sınıflandırma :
12
The association of GSTT1 deletion polymorphism with lung cancer risk among Chinese population: evidence based on a cumulative meta-analysis
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Dergi Makalesi
Open Access
Kaynak :
Directory of Open Access Journals (DOAJ)
Dergi:
OncoTargets and Therapy
Yazar(lar) :
Wang Y , Yang H , Wang H
Yıl :
2015
Wang H
Yayıncı Web Sitesi
Kaydet Alıntıla
Yadong Wang,1 Haiyan Yang,2 Haiyu Wang11Department of Toxicology, Henan Center for Disease Control and Prevention, Zhengzhou, People’s Republic of China; 2Department of Epidemiology, School of Public Health, Zhengzhou University, Zhengzhou, People’s Republic of ChinaObjective: Previous studies investigating the relationship between glutathione S-transferase T1 (GSTT1) gene deletion polymorphism and lung cancer risk among Chinese population produced inconsistent results. To obtain a precise conclusion, we performed this meta-analysis to evaluate the association between GSTT1 deletion polymorphism and lung cancer risk among Chinese population.Methods: The databases of Medline/PubMed, Embase, Web of Science, Wanfang Med Online, and Chinese National Knowledge Infrastructure were searched. The strength of the association was assessed by odds ratio (OR) with 95% confidence intervals (95% CI).Results: Overall, we found an increased lung cancer risk among subjects carrying GSTT1 null genotype compared with those carrying present genotype (OR =1.31, 95% CI: 1.12–1.52) on the basis of 20 studies with 3,351 cases and 4,683 controls. We also observed an increased risk of lung cancer among subjects carrying GSTT1 null genotype compared with those carrying present genotype in stratified analyses (OR =1.31, 95% CI: 1.11–1.55 for healthy subjects-based control; OR =2.29, 95% CI: 1.84–2.85 for squamous cell carcinoma and OR =1.47, 95% CI: 1.22–1.77 for adenocarcinoma, respectively).Conclusion: This meta-analysis suggested that GSTT1 deletion polymorphism might contribute to lung cancer risk among Chinese population.Keywords: lung cancer, risk, GSTT1, polymorphism, meta-analysis, Chinese
ISSN: 1178-6930
Cilt: 2015
Sayı: default
Sayfa: 2875 - 2882
Sınıflandırma :
13
MiR-216b suppresses colorectal cancer proliferation, migration, and invasion by targeting SRPK1
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Dergi Makalesi
Open Access
Kaynak :
Directory of Open Access Journals (DOAJ)
Dergi:
OncoTargets and Therapy
Yazar(lar) :
Yao YF , Li QR , Wang H
Yıl :
2018
Wang H
Yayıncı Web Sitesi
Kaydet Alıntıla
Yanfen Yao,1 Qiaorong Li,1 Hong Wang2 1Department of Intensive Care Unit, Shandong Provincial Third Hospital, Jinan, People’s Republic of China; 2Department of General Surgery, Shandong Provincial Third Hospital, Jinan, People’s Republic of China Background: MiR-216b has been reported to be involved in the development of some cancers, however, the role of miR-216b in colorectal cancer (CRC) remains unclear.Purpose: This study aimed to investigate the mechanism underlying miR-216b-induced CRC development.Methods: We detected the expression of miR-216b in 80 cases of CRC tissues and cell lines, and further analyzed the association between miR-216b and clinical pathological indicators as well as prognosis. In vitro, the miR-216b overexpression cell model was established for further functional assay.Results: We demonstrated that miR-216b in CRC tissues and cell lines was markedly decreased compared with corresponding adjacent normal tissues and colonic mucosal epithelial cell line, and was obviously associated with the TNM stage, lymph node metastases, and poor overall survival as well as recurrence-free survival. Furthermore, we found that miR-216b inhibited cell proliferation, cell cycle, migration, and invasion by targeting 3'-UTR of SRPK1. Besides, SRPK1 over-expression reversed miR-216b-inhibited cell proliferation, migration and invasion, while SRPK1 inhibition aggravated these effects.Conclusions: We identified that miR-216b suppresses colorectal cancer proliferation, migration and invasion by targeting SRPK1, which shed light on how miR-216b functions in CRC pathogenesis. Keywords: MiR-216b, SRPK1, colorectal cancer, proliferation, migration, invasion
Anahtar Kelimeler : MiR-216b, SRPK1, Colorectal Cancer, Proliferation, Invasion
ISSN: 1178-6930
Cilt: 11
Sayfa: 1671 - 1681
Sınıflandırma :
14
Forskolin exerts anticancer roles in non-Hodgkin’s lymphomas via regulating Axin/β-catenin signaling pathway
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Dergi Makalesi
Open Access
Kaynak :
Directory of Open Access Journals (DOAJ)
Dergi:
Cancer Management and Research
Yazar(lar) :
Wang H , Lou C , Ma N
Yıl :
2019
Wang H
Yayıncı Web Sitesi
Kaydet Alıntıla
Hailei Wang,1 Chunyan Lou,1 Na Ma2 1Department of Pediatrics, Huaihe Hospital of Henan University, Kaifeng, Henan, China; 2Department of Neurology, Henan Kaifeng Children’s Hospital, Kaifeng, Henan, China Background: Non-Hodgkin’s lymphomas (NHLs) account for 85% of lymphomas, which are characterized by high-degree malignancy, rapid progress, and even invasion into central nervous system in pediatric patients. Although the cure rate of pediatric NHL has improved, some patients have still underwent recurrence or death. This study focuses on the effects and mechanism of forskolin on the progression of NHL, aiming to find efficient therapy methods for pediatric NHL.Methods: MTT, flow cytometry and mice tumor bearing experiments were used to evaluate the effects of forskolin on NHL cell proliferation, apoptosis and tumorigenesis. Western blotting and RT-PCR assays were used to detect protein and mRNA expression. Immunohistochemistry technology was recruited to analyze Ki-67 expression in tumor tissues. Results: Forskolin significantly increased the expression of cleaved caspase-3/9 in both NHL Toledo and NK-92 cell lines, and inhibited cell growth. Besides, forskolin obviously reduced the expression of β-catenin protein, promoted its ubiquitination, enhanced its transportation from nuclear to cytoplasm, as well as decreased the expression of its downstream oncogenes c-myc and cyclin D1 through upregulating Axin expression and stability and inhibiting Axin ubiquitination. Moreover, forskolin enhanced the effects of SP600125, an inhibitor of c-Jun N-terminal kinase signaling on cell apoptosis promotion and tumorigenesis inhibition via Axin-induced β-catenin signaling repression. Conclusion:The current study clarifies that forskolin can inhibit the progression of NHL through Axin-mediated inhibition of β-catenin signaling. Moreover, forskolin improves the effects of SP600125 on cell apoptosis enhancement and tumorigenesis inhibition of NHL cells. These findings provide theoretical foundation of serving forskolin as a new effective therapeutic drug for pediatric NHL. Keywords: forskolin, SP600125, Axin, β-catenin, carcinogens
Anahtar Kelimeler : Forskolin, SP600125, beta-catenin, Non-Hodgkinu2019s lymphomas
ISSN: 1179-1322
Cilt: 11
Sayfa: 1685 - 1696
Sınıflandırma :
15
LncRNA PVT1 Regulates TRPS1 Expression in Breast Cancer by Sponging miR-543
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Dergi Makalesi
Open Access
Kaynak :
Directory of Open Access Journals (DOAJ)
Dergi:
Cancer Management and Research
Yazar(lar) :
Wang H , Huang Y , Yang Y
Yıl :
2020
Wang H
Yayıncı Web Sitesi
Kaydet Alıntıla
Hongtao Wang,1,* Yuanli Huang,2,* Yuanrong Yang1 1Department of Pharmacy, The Second Clinical Medical College, Yangtze University, Jingzhou 434020, People’s Republic of China; 2Department of Galactophore, The Second Clinical Medical College, Yangtze University, Jingzhou 434020, People’s Republic of China*These authors contributed equally to this work.Correspondence: Yuanrong Yang Email yangyuanrong_yzu@163.comBackground: Breast cancer is the most common female malignancy with high invasion and metastasis abilities. Studies have shown that long non-coding RNA (lncRNA) plasmacytoma variant translocation 1 gene (PVT1) is an oncogene and is positively correlated with progression and metastasis of breast tumors. However, the detailed mechanism of PVT1 in breast cancer tumorigenesis is not fully understood.Methods: Real-time polymerase quantitative chain reaction (RT-qPCR) was performed to identify the expression levels of PVT1, miR-543 and trichorhinophalangeal syndrome-1 gene (TRPS1) in breast cancer tissues and cells. Cell proliferation was measured by plate clone formation and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazol-3-ium bromide (MTT) assay. Apoptosis and motility of MCF-7 and MDA-MB-436 cells were assessed with flow cytometry assay and transwell migration and invasion analyses, respectively. In addition, a model was established to probe the function of PVT1 silencing in vivo. The target relationship among PVT1, miR-543 or TRPS1 was confirmed by dual-luciferase reporter analysis, RNA immunoprecipitation (RIP) and RNA pull down assays. The protein expression level of TRPS1 was evaluated with Western blot assay.Results: PVT1 expression was upregulated in breast cancer tissues and cell lines. In addition, PVT1 silencing inhibited breast cancer cell growth and motility, while increased apoptosis. Meanwhile, the effects of PVT1 or miR-543 could be reversed by introducing overexpressed plasmid of miR-543 or TRPS1 in breast cancer cell lines, respectively.Conclusion: Knockdown of PVT1 repressed breast cancer cell growth and motility, and induced apoptosis in vitro and reduced tumor volume and weight in vivo. Mechanically, the overexpression of PVT1 enhanced TRPS1 level by negatively targeted miR-543 in breast cancer.Keywords: LncRNA PVT1, miR-543, TRPS1, breast cancer
Anahtar Kelimeler : lncrna pvt1, mir-543, trps1, breast cancer
ISSN: 1179-1322
Cilt: 12
Sayfa: 7993 - 8004
Sınıflandırma :
16
SP1-Mediated Upregulation of lncRNA LINC01614 Functions a ceRNA for miR-383 to Facilitate Glioma Progression Through Regulation of ADAM12
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Dergi Makalesi
Open Access
Kaynak :
Directory of Open Access Journals (DOAJ)
Dergi:
OncoTargets and Therapy
Yazar(lar) :
Wang H , Wu J , Guo W
Yıl :
2020
Wang H
Yayıncı Web Sitesi
Kaydet Alıntıla
Hao Wang,1 Jiang Wu,2 Wei Guo1 1Department of Neurosurgery, Shenzhen People’s Hospital, The Second Clinical Medical College of Jinan University, Shenzhen, Guangdong, People’s Republic of China; 2Department of Neurosurgery, Hebei General Hospital, Shijiazhuang, Hebei, People’s Republic of ChinaCorrespondence: Wei GuoDepartment of Neurosurgery, Shenzhen People’s Hospital, The Second Clinical Medical College of Jinan University, No. 1017, Dongmen North Road, Shenzhen, Guangdong, People’s Republic of ChinaEmail lanmlw7761@sina.comBackground: Long non-coding RNAs (lncRNAs) play an imperative role in tumorigenesis, but few lncRNAs have been functionally characterized in glioma. The aim of the present study was to identify the role of long non-coding RNA LINC01614 (LINC01614) in glioma development and explore the underlying mechanisms of LINC01614/miR-383/ADAM12 axis.Patients and Methods: LncRNA expression in glioma specimens was measured by lncRNA microarray and qRT-PCR. The prognostic value of LINC01614 expression was statistically analyzed in 112 glioma patients. Loss-of-function experiments were conducted to investigate the biological functions of LINC01614 in vitro. Luciferase analyses, ChIP assays, and RNA pull-down were performed to determine the underlying LINC01614 mechanisms.Results: We identified a novel glioma-related lncRNA LINC01614 by analyzing TCGA datasets. The distinct upregulation of LINC01614 was observed in both glioma specimens and cell lines using RT-PCR. We also observed that LINC01614 upregulation was induced by nuclear transcription factor SP1. Clinical assays revealed that high levels of LINC01614 were associated with KPS, WHO grade and shorter overall survival of glioma patients. Multivariate analysis further confirmed that LINC01614 was an independent prognostic marker for glioma patients. Besides, functional assays displayed that silence of LINC01614 knockdown distinctly inhibited cell growth, migration and invasion and promoted cell apoptosis in glioma cells. LINC01614 expression was enriched in the cytoplasm of glioma cells. Mechanistic investigation revealed that LINC01614 functioned as a competing endogenous RNA to upregulate a disintegrin and metalloproteinase 12 (ADAM12) by sponging miR-383.Conclusion: Overall, these findings showed that SP1-induced upregulation of LINC01614 promoted glioma malignant progression via modulating the miR-383/ADAM12 axis, which may provide a promising therapy for glioma.Keywords: lncRNA LINC01614, miR-383, ADAM12, prognosis, metastasis, glioma
Anahtar Kelimeler : lncrna linc01614, mir-383, adam12, prognosis, metastasis, glioma.
ISSN: 1178-6930
Cilt: 13
Sayfa: 4305 - 4318
Sınıflandırma :
17
miR-140-5p Alleviates The Aggressive Progression Of Wilms’ Tumor Through Directly Targeting TGFBR I Gene Retraction
Dergi Makalesi

Dergi Makalesi
Open Access
Kaynak :
Directory of Open Access Journals (DOAJ)
Dergi:
Cancer Management and Research
Yazar(lar) :
Wang H , Lou C , Ma N
Yıl :
2019
Wang H
Yayıncı Web Sitesi
Kaydet Alıntıla
Wang H, Lou C, Ma N. miR-140-5p alleviates the aggressive progression of Wilms’ tumor through directly targeting TGFBR I gene. Cancer Manage Res. 2019;11:1641–1651.The Editor-in-Chief and Publisher of Cancer Management and Research wish to retract the published article.Following publication, concerns were raised to the Editor in-Chief regarding the Wilms’ tumor cell lines described in the study.Upon investigation it was found the human Wilms’ tumor cell lines used in the present study, G-401 and SK-NEP-1, had been wrongly attributed and are not, in fact, Wilms’ tumor cell lines as claimed. The cell line, G-401, has been shown to be a rhabdoid tumor cell line of the kidney and has been reclassified, accordingly, in the American Tissue Culture Collection (ATCC) (https://www.atcc.org/Products/All/CRL-1441.aspx). The cell line, SK-NEP-1 has also been investigated and was found to have a close relationship with the Ewing sarcoma cell line, not theWilms’ tumor cell line as previously indicated.Based on this information the Editor-in-Chief has determined the results and findings of the present study are no longer valid.This retraction relates to this paper
ISSN: 1179-1322
Cilt: 11
Sayfa: 8605 - 8606
Sınıflandırma :
18
Mst1-Hippo pathway triggers breast cancer apoptosis via inducing mitochondrial fragmentation in a manner dependent on JNK–Drp1 axis
Dergi Makalesi

Dergi Makalesi
Open Access
Kaynak :
Directory of Open Access Journals (DOAJ)
Dergi:
OncoTargets and Therapy
Yazar(lar) :
Ouyang H , Zhou E , Wang H
Yıl :
2019
Wang H
Yayıncı Web Sitesi
Kaydet Alıntıla
Hui Ouyang, Enxiang Zhou, Huan Wang Department of Breast and Thyroid Surgery, The Second Xiangya Hospital of Central South University, Changsha, Hunan 410011, China Background and objective: Mst1-Hippo pathway and mitochondrial fragmentation participate in the progression of several types of cancers. However, their roles in breast cancer requires investigation. The aim of our study is to determine whether Mst1 overexpression regulates the viability of breast cancer cells via modulating mitochondrial fragmentation. Materials and methods: TUNEL staining, MTT assay and Western blotting were used to detect cancer cell death. Adenovirus-loaded Mst1 was transfected into cells to overexpress Mst1. Mitochondrial fragmentation was observed via immunofluorescence staining and Western blotting. Pathway blocker was used to detect whether Mst1 modulated cell death and mitochondrial fragmentation via JNK signaling pathway. Results: Our data showed that Mst1 overexpression promoted breast cancer cell death in a manner dependent on mitochondrial apoptosis. Mitochondrial oxidative stress, energy metabolism disorder, mitochondrial cyt-c liberation and mitochondrial apoptosis activation were observed after Mst1 overexpression. Furthermore, we demonstrated that Mst1 overexpression activated mitochondrial stress via triggering Drp1-related mitochondrial fragmentation, and that inhibition of Drp1-related mitochondrial fragmentation abrogated the proapoptotic effect of Mst1 overexpression on breast cancer cells. To this end, we found that Mst1 modulated Drp1 expression via the JNK signaling pathway, and that blockade of the JNK pathway attenuated mitochondrial stress and repressed apoptosis in Mst1-overexpressed cells. Conclusion: Altogether, our results identified a tumor suppressive role for Mst1 overexpression in breast cancer via activation of the JNK–Drp1 axis and subsequent initiation of fatal mitochondrial fragmentation. Given these findings, strategies to enhance Mst1 activity and elevate the JNK–Drp1–mitochondrial fragmentation cascade have clinical benefits for patients with breast cancer. Keywords: breast cancer, mitochondrial fragmentation, Mst1, JNK–Drp1 signaling pathway, mitochondrial dysfunction
Anahtar Kelimeler : breast cancer, mitochondrial fragmentation, JNK-Drp1 signaling pathway, mitochondrial dysfunction
ISSN: 1178-6930
Cilt: 12
Sayfa: 1147 - 1159
Sınıflandırma :
Biyotıp %100
Apoptoz %66
Biyotıp %28
19
Identification of Candidate Genes and Therapeutic Agents for Light Chain Amyloidosis Based on Bioinformatics Approach
Dergi Makalesi

Dergi Makalesi
Open Access
Kaynak :
Directory of Open Access Journals (DOAJ)
Dergi:
Pharmacogenomics and Personalized Medicine
Yazar(lar) :
Bai W , Wang H , Bai H
Yıl :
2020
Wang H
Yayıncı Web Sitesi
Kaydet Alıntıla
Wenxiang Bai,1,2,* Honghua Wang,1,* Hua Bai1,3 1Comprehensive Cancer Center, Xiangshui People’s Hospital, Xiangshui 224600, People’s Republic of China; 2Department of Respiratory Medicine, Xiangshui People’s Hospital, Xiangshui, 224600, People’s Republic of China; 3Department of Hematology, The Affiliated Drum Tower Hospital of Nanjing University Medical School, Nanjing 210008, People’s Republic of China*These authors contributed equally to this workCorrespondence: Hua BaiComprehensive Cancer Center, Xiangshui People’s Hospital, Xiangshui 224600, People’s Republic of ChinaEmail baihua92@126.comObjective: Systemic amyloid light chain (AL) amyloidosis is a rare plasma cell disease. However, the regulatory mechanisms of AL amyloidosis have not been thoroughly uncovered, identification of candidate genes and therapeutic agents for this disease is crucial to provide novel insights into exploring the regulatory mechanisms underlying AL amyloidosis.Methods: The gene expression profile of GSE73040, including 9 specimens from AL amyloidosis patients and 5 specimens from normal control, was downloaded from GEO datasets. Differentially expressed genes (DEGs) were sorted with regard to AL amyloidosis versus normal control group using Limma package. The gene enrichment analyses including GO and KEGG pathway were performed using DAVID website subsequently. Furthermore, the protein–protein interaction (PPI) network for DEGs was constructed by Cytoscape software and STRING database. DEGs were mapped to the connectivity map datasets to identify potential molecular agents of AL amyloidosis.Results: A total of 1464 DEGs (727 up-regulated, 737 down-regulated) were identified in AL amyloidosis samples versus control samples, these dysregulated genes were associated with the dysfunction of ribosome biogenesis and immune response. PPI network and module analysis uncovered that several crucial genes were defined as candidate genes, including ITGAM, ITGB2, ITGAX, IMP3 and FBL. More importantly, we identified the small molecular agents (AT-9283, Ritonavir and PKC beta-inhibitor) as the potential drugs for AL amyloidosis.Conclusion: Using bioinformatics approach, we have identified candidate genes and pathways in AL amyloidosis, which can extend our understanding of the cause and molecular mechanisms, and these crucial genes and pathways could act as biomarkers and therapeutic targets for AL amyloidosis.Keywords: light chain amyloidosis, bioinformatics approach, differentially expressed genes, candidate genes, therapeutic agent
Anahtar Kelimeler : light chain amyloidosis, bioinformatics approach, differentially expressed genes, candidate genes, therapeutic agent
ISSN: 1178-7066
Cilt: 12
Sayfa: 387 - 396
Sınıflandırma :
20
A DNA vaccine encoding mutated HPV58 mE6E7-Fc-GPI fusion antigen and GM-CSF and B7.1
Dergi Makalesi

Dergi Makalesi
Open Access
Kaynak :
Directory of Open Access Journals (DOAJ)
Dergi:
OncoTargets and Therapy
Yazar(lar) :
Wang H , Yu J , Li L
Yıl :
2015
Wang H
Yayıncı Web Sitesi
Kaydet Alıntıla
He Wang,1 Jiyun Yu,2 Li Li1 1Department of Gynecologic Oncology, Affiliated Tumor Hospital of Guangxi Medical University, Nanning, Guangxi, 2Institute of Basic Medical Sciences, Academy of Military Medical Sciences, Beijing, People’s Republic of China Background: Persistent infection with high-risk human papillomavirus (HPV) is a predominant cause of cervical cancer, and HPV58 is the third most common virus detected in the patients with cervical cancer in Asia. E6 and E7 are the viral oncogenes which are constitutively expressed in HPV-associated tumor cells and can be used as target antigens for related immunotherapy. In this study, we modified the HPV58 E6 and E7 oncogenes to eliminate their oncogenic potential and constructed a recombinant DNA vaccine that coexpresses the sig-HPV58 mE6E7-Fc-GPI fusion antigen in addition to granulocyte-macrophage colony-stimulating factor (GM-CSF) and B7.1 as molecular adjuvants (PVAX1-HPV58 mE6E7FcGB) for the treatment of HPV58 (+) cancer. Methods: PVAX1-HPV58 mE6E7FcGB recombinant DNA vaccine was constructed to express a fusion protein containing a signal peptide, a modified HPV58 mE6E7 gene, and human IgG Fc and glycosylphosphatidylinositol (GPI)-anchoring sequences using the modified DNA vaccine vector PVAX1-IRES-GM/B7.1 that coexpresses GM-CSF, and B7.1. C57BL/6 mice were challenged by HPV58 E6E7-expressing B16-HPV58 E6E7 cells, followed by immunization by PVAX1-HPV58 mE6E7FcGB vaccine on days 7, 14, 21 after tumor challenge. The cellular immune responses in immunized mice were assessed by measuring IFN-γ production in splenocytes upon stimulation by HPV58 E6E7-GST protein and the lysis of B16-HPV58 E6E7 target cells by splenocytes after restimulation with HPV58 E6E7-GST protein. The antitumor efficacy was evaluated by monitoring the growth of the tumor. Results: PVAX1-HPV58 mE6E7FcGB elicited varying levels of IFN-lsgdB58onn T-cell immune responses and lysis of target cell in mice in response to the recombinant antigen HPV58 E6E7-GST. Furthermore, the vaccine also induced antitumor responses in the HPV58 (+) B16-HPV58 E6E7 tumor challenge model as evidenced by delayed tumor development. Conclusion: The recombinant DNA vaccine PVAX1-HPV58 mE6E7FcGB efficiently generates cellular immunity and antitumor efficacy in immunized mice. These data provide a basis for the further study of this recombinant vaccine as a potential candidate vaccine. Keywords: human papillomavirus type 58, E6 gene, E7 gene, DNA vaccine, immunogenicity
ISSN: 1178-6930
Cilt: 2015
Sayı: default
Sayfa: 3067 - 3077
Sınıflandırma :
Biyotıp %100
Viroloji %91
21
Breaking barriers: insight into the pathogenesis of neovascular age-related macular degeneration
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Dergi Makalesi
Open Access
Kaynak :
Directory of Open Access Journals (DOAJ)
Dergi:
Eye and Brain
Yazar(lar) :
Hartnett ME , Wittchen ES , Wang H
Yıl :
2011
Wang H
Yayıncı Web Sitesi
Kaydet Alıntıla
Haibo Wang1, Erika S Wittchen2, M Elizabeth Hartnett11Department of Ophthalmology, John A Moran Eye Center, University of Utah, Salt Lake City, UT; 2Department of Cell and Developmental Biology, University of North Carolina at Chapel Hill, Chapel Hill, NC, USAAbstract: Neovascular age-related macular degeneration (AMD) is a leading cause of central visual acuity loss in a growing segment of the population, those over the age of 60 years. Treatment has improved over the last decade, with the availability of agents that inhibit the bioactivity of vascular endothelial growth factor (VEGF), but it is still limited, because of tachyphylaxis and potential risk and toxicity of anti-VEGF agents. The authors have sought to understand the mechanisms of choroidal endothelial cell (CEC) activation and transmigration of the retinal pigment epithelium (RPE) and of RPE barrier dysfunction, events preceding vision-threatening neovascular AMD. The authors developed physiologically relevant human RPE and CEC coculture and transmigration models that have been important in helping to understand causes of events in human neovascular AMD. The authors can control for interactions between these cells and can separately assess activation of signaling pathways in each cell type relevant during CEC transmigration. Using these models, it was found that VEGF, particularly the cell-associated VEGF splice variant VEGF189, accounts for about 40% of CEC transmigration across the RPE. This percentage is in the range of similar reports following clinical inhibition of VEGF in neovascular AMD. RPE VEGF189 working through CEC VEGF receptor 2 activates the small guanosine triphosphatase (GTPase) of the Rho family, Rac1, in CECs, which in turn facilitates CEC transmigration. Conversely, inhibition of Rac1 activity prevents CEC transmigration. Once activated, Rac1 aggregates with subunits of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, resulting in the generation of reactive oxygen species. Activated NADPH oxidase increases choroidal neovascularization in animal models of laser-induced injury. Rac1 is also downstream of the eotaxin-CCR3 pathway, another pathway important in human neovascular AMD. Studies also suggest that active Ras-related protein 1 (Rap1), another small GTPase, in RPE can strengthen the RPE barrier integrity and can resist CEC transmigration of the RPE, suggesting Rap1 activation may be another potential target for preventing neovascular AMD.Keywords: choroidal endothelial cell (CEC), Rac1/Rap1 GTPase, retinal pigment epithelium (RPE), vascular endothelial growth factor (VEGF), NADPH oxidase 
ISSN: 1179-2744
Cilt: 2011
Sayı: default
Sayfa: 19 - 28
Sınıflandırma :
22
miR-598 acts as a tumor suppressor in human gastric cancer by targeting IGF-1R
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Dergi Makalesi
Open Access
Kaynak :
Directory of Open Access Journals (DOAJ)
Dergi:
OncoTargets and Therapy
Yazar(lar) :
Liu N , Yang H , Wang H
Yıl :
2018
Wang H
Yayıncı Web Sitesi
Kaydet Alıntıla
Na Liu,1 Hua Yang,2 Hong Wang3 1Intensive Care Unit, Shandong Provincial Third Hospital, Shandong, China; 2Intensive Care Unit, Chiping County People’s Hospital, Shandong, China; 3Department of General Surgery, Shandong Provincial Third Hospital, Shandong, China Background: In recent years, the aberrant expression of miR-598 in tumorigenesis has been demonstrated, as well as the fact that the IGF-1R pathway is also involved in the development of human gastric cancer (GC). The present study aimed to investigate the molecular mechanisms underlying miR-598-regulated IGF-1R expression in human GC.Materials and methods: We analyzed the expression of miR-598 and IGF-1R in GC samples and cells, and evaluated the clinical significance of miR-598 and IGF-1R in GC patients. Furthermore, in vitro and in vivo assays were used to investigate the molecular mechanisms of miR-598 and IGF-1R.Results: miR-598 expression was frequently downregulated in GC tissues and cells, and significantly correlated with poor prognosis, vascular invasion, TNM stage, and lymph node metastases as well as IGF-1R expression. The overexpression of miR-598 obviously inhibited cell proliferation, migration, invasion, and induced cell cycle arrest in the G1/S phase, and increased the apoptosis of GC cells. The overexpression of miR-598 also significantly inhibited ERK1/2 and Akt phosphorylation level. In vivo assay validated the inhibitory effect of miR-598 on tumor growth. Further studies showed that miR-598 inhibited IGF-1R protein expression by directly targeting its 3´-UTR. Besides, over-expression of IGF-1R reversed the inhibitory effects of miR-598, while suppression of IGF-1R expression showed inverse effects. Conclusion: miR-598 suppresses GC cell proliferation, migration and invasion by directly targeting IGF-1R expression. Thus, miR-598 may be a useful target for GC patients. Keywords: miR-598, IGF-1R, gastric cancer, proliferation, migration, invasion suppressor
Anahtar Kelimeler : MiR-598, IGF-1R, Gastric Cancer, Proliferation, Migration, Invasion Suppressor
ISSN: 1178-6930
Cilt: 11
Sayfa: 2911 - 2923
Sınıflandırma :
23
Effects of laminating and co-firing conditions on the performance of anode-supported Ce0.8Sm0.201.9 film electrolyte
Dergi Makalesi

Dergi Makalesi
Open Access
Kaynak :
Directory of Open Access Journals (DOAJ)
Dergi:
Science of Sintering
Yazar(lar) :
Li X. , Lu J. , Wang H.
Yıl :
2011
Wang H.
Yayıncı Web Sitesi
Tam Metin
Kaydet Alıntıla
In order to evaluate the laminating and co-firing technique on the performance of anode-supported Ce0.8Sm0.2O1.9 (SDC) film electrolyte and its single cell, NiO-YSZ and NiOSDC anode-supported SDC film electrolytes were fabricated by laminating 24 sheets of anode plus one sheet of electrolyte and co-firing. La0.4Sr0.6Co0.2Fe0.8O3-δ (LSCF)-SDC cathode was coated on the SDC electrolytes to form a single cell. The lamination was tried at different laminating temperatures and pressures and the co-firing was carried out at different temperatures. The results showed that the laminating temperature should above the glass transition temperature (Tg) of the binder. The laminating pressure of 70 MPa resulted in warp of the samples. The best co-firing temperature of the anode-supported SDC film electrolyte was 1400°C. The SDC film electrolyte formed well adherence to the anode. The NiO-YSZ anode had larger flexural strength than the NiO-SDC anode. The NiO-YSZ anode-supported SDC film electrolyte single cell had an open circuit voltage of 0.803 V and a maximum power density of 93.03 mW/cm2 with hydrogen as fuel at 800°C.
DOI : 10.2298/SOS1103305L
Anahtar Kelimeler : Ce0.8Sm0.2O1.9, laminating, co-firing, condition, anode-supported SOFC
Cilt: 43
Sayı: 3
Sayfa: 305 - 312
Sınıflandırma :
24
NLRP3 Inflammasome Mediated Interleukin-1β Production in Cancer-Associated Fibroblast Contributes to ALA-PDT for Cutaneous Squamous Cell Carcinoma
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Dergi Makalesi
Open Access
Kaynak :
Directory of Open Access Journals (DOAJ)
Dergi:
Cancer Management and Research
Yazar(lar) :
Nie S , Wang X , Wang H
Yıl :
2019
Wang H
Yayıncı Web Sitesi
Kaydet Alıntıla
Shu Nie,1 Xiuli Wang,2 Hongwei Wang1 1Department of Dermatology, Huadong Hospital Affiliated to Fudan University, Shanghai 200040, People’s Republic of China; 2Institute of Photomedicine, Shanghai Skin Disease Hospital, Tongji University School of Medicine, Shanghai 200443, People’s Republic of ChinaCorrespondence: Hongwei WangDepartment of Dermatology, Huadong Hospital Affiliated to Fudan University, Shanghai 200040, People’s Republic of ChinaEmail hongweiwang2017@163.comXiuli WangInstitute of Photomedicine, Shanghai Skin Disease Hospital, Tongji University School of Medicine, Shanghai 200443, People’s Republic of ChinaEmail wangxiuli_1400023@tongji.edu.cnBackground: Long-term tumor control following PDT is a result of its direct effect on tumor and vasculature in combination with induction of inflammatory-reactions upregulating the immune system. When PDT induces necrosis of tumors and vascular system, an immune cascade can be initiated to release all kinds of cytokines including IL1β. This further leads to the activation of inflammatory-cells and hence death of tumor cells.Methods: Ultraviolet irradiation was used to induce cSCC mice model, gene chip was used to screen inflammatory cytokines, qPCR, ELISA and implanted tumor mice model were used to verify the changes and important role of interleukin-1β, and WB preliminarily explored the production mechanism of interleukin-1β.Results: Inflammatory cytokines and receptors transcript screening identify IL1r1 as the top4. After ALA-PDT, IL1r1 and IL1β increased in patients’ biopsies, principally in mesenchymal cells. In vivo, the inhibition of ALA-PDT on tumor growth of cutaneous squamous cell carcinoma (cSCC) mice in the group with intralesional injection of anti-IL1β mAb or caspase1-inhibitor was significantly weaker than the control groups. Furthermore, NLRP3-inflammasome and p-p65/p65 were elevated after ALA-PDT mediated IL1β production in cancer-associated-fibroblasts.Discussion: By means of activating NLRP3-inflammasome with IL1β production in CAFs, PDT stimulates local acute-inflammatory-response, which further promotes PDT effect for cSCC.Keywords: cancer-associated fibroblast, photodynamic therapy, interleukin-1β, NLRP3-inflammasome, squamous cell carcinoma
Anahtar Kelimeler : cancer associated fibroblast, photodynamic therapy, interleukin-1β, nlrp3-inflammasome, squamous cell carcinoma
ISSN: 1179-1322
Cilt: 11
Sayfa: 10257 - 10267
Sınıflandırma :
25
miR-140-5p alleviates the aggressive progression of Wilms’ tumor through directly targeting TGFBR1 gene
Dergi Makalesi

Dergi Makalesi
Open Access
Kaynak :
Directory of Open Access Journals (DOAJ)
Dergi:
Cancer Management and Research
Yazar(lar) :
Wang H , Lou C , Ma N
Yıl :
2019
Wang H
Yayıncı Web Sitesi
Kaydet Alıntıla
Hailei Wang,1 Chunyan Lou,1 Na Ma2 1Department of Pediatrics, Huaihe Hospital of Henan University, Kaifeng, Henan, China; 2Department of Neurology, Henan Kaifeng Children’s Hospital, Kaifeng, Henan, China Background and objective: Although many miRNAs are identified to be deregulated and play vital roles in the progression of Wilms’ tumor (WT), there are still a large number of miRNAs are waiting for us to explore. The purpose of the present study is to investigate the different expressing profiles of miRNAs in WT tissues and the adjacent normal tissues, and probe the effects and mechanism of a certain miRNA among the different expressing miRNAs. Methods: miRNA microarray was recruited to assess the differently expressed miRNAs in WT tissues and normal tissues, which was further verified by RT-PCR. Receiver operating characteristic curves were performed to calculate the specificity and sensitivity of miRNAs in the diagnose of WT. CCK-8, flow cytometry, wound healing, transwell chamber and tumor-burdened assays were used to assess cell growth, apoptosis, migration, invasion and tumorigenesis. Luciferase report assay was used to evaluate the interaction between miR-140-5p and TGFBR1.Results: A total of 34 miRNAs were abnormally expressed in the WT tissues, among which, miR-140-5p was identified to be obviously down-regulated in WT tissues, and the AUC of it was 0.961. Besides, we found that patients with miR-140-5p low expression always had a shorter overall survival and more aggressive clinical features, such as bigger tumor size (P=0.002), higher pathological stage (P=0.003) and higher occurrence rate of lymph node metastasis (P=0.009) than those in patients with miR-140-5p high expression. Moreover, luciferase reporter assay showed that TGFBR1 was the direct target of miR-140-5p, which was negatively regulated by miR-140-5p and was highly expressed in WT tissues. Furthermore, knockdown of miR-140-5p obviously enhanced the proliferation and tumorigenesis and repressed the apoptosis of G401 cells, and these effects were all abolished when TGFBR1 was down-regulated. Conclusion: The present study illustrates that miR-140-5p functions as a tumor suppressor in the occurrence and development of WT via targeting TGFBR1, which provides theoretical foundation for serving miR-140-5p as a new diagnosis marker even a therapeutic target for WT. Keywords: miR-140-5p, TGFBR1, Wilms’ tumor
Anahtar Kelimeler : miR-140-5p, TGFBR1, Wilms tumor
ISSN: 1179-1322
Cilt: 11
Sayfa: 1641 - 1651
Sınıflandırma :
26
HJC0152, a novel STAT3 inhibitor with promising anti-tumor effect in gastric cancer
Dergi Makalesi

Dergi Makalesi
Open Access
Kaynak :
Directory of Open Access Journals (DOAJ)
Dergi:
Cancer Management and Research
Yazar(lar) :
Jiang X , Wu M , Xu Z , Wang H , Wang H , Yu X , Li Z , Teng L
Yıl :
2018
Wang H Wang H
Yayıncı Web Sitesi
Kaydet Alıntıla
Xiaoxia Jiang,1,2 Mengjie Wu,1,2 Zhenzhen Xu,1,2 Haohao Wang,1,2 Haiyong Wang,1,2 Xiongfei Yu,1 Zhongqi Li,1 Lisong Teng1,2 1Department of Surgical Oncology, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, People’s Republic of China; 2Key Laboratory of Precision Diagnosis and Treatment for Hepatobiliary and Pancreatic Tumor of Zhejiang Province, Hangzhou, People’s Republic of China Background: Aberrant activation of the signal transducer and activator of transcription 3 (STAT3) is frequently seen in patients with gastric cancer (GC), and is generally associated with worse prognosis. HJC0152, a novel STAT3 inhibitor, has shown significant anti-tumor effects in several cancers, although its role in GC remains to be clarified. Methods: The effect of HJC0152 on STAT3 signaling pathway and the biological behaviors of GC cells were evaluated through in vitro and/or in vivo experiments. Meanwhile, RNA sequence analysis was used to further explore its potential anti-tumor mechanisms.Results: HJC0152 inhibited the expression of activated STAT3 and its downstream target genes (c-Myc and clyclinD1) in GC cells, and restrained tumor growth in vivo. HJC0152 treatment induced apoptosis in the STAT3 hyper-activated AGS and MKN45 cell lines, along with down-regulation of survivin and Mcl1, and up-regulation of cleaved-poly(ADP-ribose) polymerase. Moreover, HJC0152 markedly inhibited migration and invasion of these cells. Finally, RNA sequence analysis and protein expression analyses showed that in addition to STAT3 suppression, HJC0152 also exerts its anti-tumor effects at least partly via the mitogen-activated protein kinases pathway. Conclusion: Our findings highlight that HJC0152 is a promising therapeutic agent for GC. Keywords: gastric cancer, inhibitor, HJC0152, STAT3, MAPK
Anahtar Kelimeler : gastric cancer, inhibitor, HJC0152, STAT3
ISSN: 1179-1322
Cilt: 10
Sayfa: 6857 - 6867
Sınıflandırma :
27
Prognostic Value of the Combination of CEA and Fibrinogen/Albumin Ratio in Resectable Gastric Cancer
Dergi Makalesi

Dergi Makalesi
Open Access
Kaynak :
Directory of Open Access Journals (DOAJ)
Dergi:
Cancer Management and Research
Yazar(lar) :
Zhang J , Ruan J , Wang W , Lu Y , Wang H , Yu X , Wang H , Teng L
Yıl :
2020
Wang H Wang H
Yayıncı Web Sitesi
Kaydet Alıntıla
Junbin Zhang, Jiayin Ruan, Weibin Wang, Yimin Lu, Haiyong Wang, Xiongfei Yu, Haohao Wang, Lisong Teng Department of Surgical Oncology, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, People’s Republic of ChinaCorrespondence: Haohao Wang; Lisong Teng Tel/Fax +86 57187236881Email coldhot33@126.com; lsteng@zju.edu.cnPurpose: To investigate the prognostic value of combined serum carcinoembryonic antigen (CEA) levels and fibrinogen/albumin ratio (FAR) in patients with resectable gastric cancer (GC).Introduction: This retrospective study evaluated the CEA, fibrinogen, and albumin levels and other clinicopathological features of GC patients. The prognostic significance of these factors for overall survival (OS) was assessed using Kaplan–Meier curves and univariate and multivariate Cox proportional models.Patients and Methods: A total of 267 patients were included. The optimal cutoff values of CEA and FAR were 3.2 ng/mL and 0.086, respectively. Patients were stratified into three groups based on this cutoff value: CEA-FAR=0 (CEA < 3.2 ng/mL and FAR < 0.086), CEA-FAR=1 (CEA ≥ 3.2 ng/mL or FAR ≥ 0.086), and CEA-FAR=2 (CEA ≥ 3.2 ng/mL and FAR ≥ 0.086).Results: Higher CEA-FAR was strongly associated with age, tumor size, tumor invasion, lymph node status, and TNM stage (all P< 0.05). The OS rates differed significantly between these 3 groups (88.9% vs 65.0% vs 46.9%, P< 0.001). Multivariate analysis showed that CEA-FAR was an independent prognostic factor for OS (P< 0.001). The area under the curve was larger for CEA-FAR than for either CEA or FAR alone (0.683, 0.644, and 0.669, respectively).Conclusion: Preoperative CEA-FAR could be a potential blood marker for predicting tumor progression and the prognosis of GC patients. Patients with a higher CEA-FAR should undergo extensive follow-up.Keywords: gastric carcinoma, patients, survival, risk factor
Anahtar Kelimeler : gastric carcinoma, patients, survival, risk factor
ISSN: 1179-1322
Cilt: 12
Sayfa: 2767 - 2775
28
Advances in the targeted therapy of liposarcoma
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Dergi Makalesi
Open Access
Kaynak :
Directory of Open Access Journals (DOAJ)
Dergi:
OncoTargets and Therapy
Yazar(lar) :
Guan Z , Yu X , Wang H , Wang H , Zhang J , Li G , Cao J , Teng L
Yıl :
2015
Wang H Wang H
Yayıncı Web Sitesi
Kaydet Alıntıla
Zhonghai Guan,1 Xiongfei Yu,1 Haohao Wang,1 Haiyong Wang,1 Jing Zhang,1 Guangliang Li,2 Jiang Cao,3 Lisong Teng1 1Department of Surgical Oncology, First Affiliated Hospital, College of Medicine, Zhejiang University, 2Department of Medicine Oncology, Zhejiang Cancer Hospital, 3Clinical Research Center, The 2nd Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, People’s Republic of China Abstract: Liposarcoma (LPS) is the most common type of soft-tissue sarcoma. Complete surgical resection is the only curative means for localized disease; however, both radiation and conventional cytotoxic chemotherapy remain controversial for metastatic or unresectable disease. An increasing number of trials with novel targeted therapy of LPS have provided encouraging data during recent years. This review will provide an overview of the advances in our understanding of LPS and summarize the results of recent trials with novel therapies targeting different genetic and molecular aberrations for different subtypes of LPS. Keywords: well-/dedifferentiated, myxoid/round cell, pleomorphic, soft-tissue sarcoma
ISSN: 1178-6930
Cilt: 2015
Sayı: default
Sayfa: 125 - 136
Sınıflandırma :
29
An Experimental Investigation of Transpiration Cooling. Part I: Application of an Infrared Measurement Technique
Dergi Makalesi

Dergi Makalesi
Open Access
Kaynak :
Directory of Open Access Journals (DOAJ)
Dergi:
International Journal of Rotating Machinery
Yazar(lar) :
Wang H. J. , Messner J. , Stetter H.
Yıl :
2003
Wang H. J.
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Kaydet Alıntıla
Cilt: 9
Sayı: 3
Sayfa: 153 - 161
Sınıflandırma :
30
Octaarginine-modified gold nanoparticles enhance the radiosensitivity of human colorectal cancer cell line LS180 to megavoltage radiation
Dergi Makalesi

Dergi Makalesi
Open Access
Kaynak :
Directory of Open Access Journals (DOAJ)
Dergi:
International Journal of Nanomedicine
Yazar(lar) :
Zhang XY , Wang H , Coulter JA , Yang R
Yıl :
2018
Wang H
Yayıncı Web Sitesi
Kaydet Alıntıla
Xuyang Zhang,1 Hao Wang,1 Jonathan Andrew Coulter,2 Ruijie Yang1 1Department of Radiation Oncology, Peking University Third Hospital, Beijing, China; 2School of Pharmacy, Queen’s University of Belfast, Belfast, UK Background: This study investigated the effectiveness and underpinning mechanisms of radiosensitization using octaarginine (R8)-modified gold nanoparticle–poly(ethylene glycol) (GNP-PEG-R8) in colorectal cancer cell line LS180 to megavoltage radiotherapy in vitro. Method: In-house synthesized GNP-PEG was characterized by transmission electron microscopy, dynamic light scattering, ultraviolet–visible spectrophotometry, and X-ray photoelectron spectroscopy. Inductively coupled plasma mass spectroscopy was used to quantify internalization. Direct cytotoxicity was established using the Cell Counting Kit-8, while radiosensitivity was determined using the gold standard in vitro clonogenic assay. Cell-cycle distribution, apoptosis, reactive oxygen species (ROS), and mitochondrial membrane potential (MMP) were analyzed by flow cytometry, further exploring the key mechanisms driving GNP-PEG-R8 radiosensitization. Results: The core GNP diameter was 6.3±1.1 nm (mean±SD). Following functionalization, the hydrodynamic diameter increased to 19.7±2.8 nm and 27.8±1.8 nm for GNP-PEG and GNP-PEG-R8, with respective surface plasmon resonance peaks of 515 nm and 525 nm. Furthermore, incorporation of the R8 significantly increased nanoparticle internalization compared to GNP-PEG (p<0.001) over a 1 h treatment period. Functionalized GNPs confer little cytotoxicity below 400 nM. In clonogenic assays, radiation combined with GNP-PEG-R8 induced a significant reduction in colony formation compared with radiation alone, generating a sensitizer enhancement ratio of 1.59. Furthermore, GNP-PEG-R8 plus radiation predominantly induced cell-cycle arrest in the G2/M phase, increasing G2/M stalling by an additional 10% over GNP-PEG, markedly promoting apoptosis (p<0.001). Finally, ROS levels and alterations in MMP were investigated, indicating a highly significant (p<0.001) change in both parameters following the combined treatment of GNP-PEG-R8 and radiation over radiation alone. Conclusion: R8-modified GNPs were efficiently internalized by LS180 cells, exhibiting minimal cytotoxicity. This yielded significant radiosensitization in response to megavoltage radiation. GNP-PEG-R8 may enhance radiosensitivity by arresting cell cycle and inducing apoptosis, with elevated ROS identified as the likely initiator. Keywords: gold nanoparticles, octaarginine, colorectal cancer, megavoltage radiotherapy, mechanisms, radiosensitization
Cilt: 13
Sayfa: 3541 - 3552

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