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
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 email@example.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
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
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
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 firstname.lastname@example.orgAbstract: 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
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
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
Haematophagous insect vectors of arthropod-borne viruses (arboviruses) feed repeatedly. Consequently, they can transmit arboviruses to more than one host during the same developmental stage (intra-stadial transmission). By contrast, ixodid ticks generally feed only once at each parasitic stage (larva, nymph, and adult) and hence they have only one opportunity for tickborne virus transmission per stadium (inter-stadial transmission). Under natural conditions, tick-infested hosts may die (from disease or other causes) before the ticks have completed their long period of engorgement. A laboratory model was used to investigate the consequences of premature host death on tick-borne virus transmission. We report intra-stadial transmission of Thogoto virus by the nymphal, male, and female ticks of Rhipicephalus appendiculatus. Tick-borne Thogoto virus infection caused viraemia and death of hamsters before the nymphal and adult ticks feeding on them had completed engorgement. The resulting partially fed ticks were allowed to continue engorgement on new, uninfected hosts (interrupted feeding). During feeding on the subsequent hosts, they transmitted the virus intra-stadially to susceptible hosts (hamsters), and to uninfected co-feeding ticks on non-susceptible hosts (guinea-pigs). Intra-stadial transmission, mediated by interrupted feeding, may help explain outbreaks of rapid and fatal tick-borne viral diseases, and the epidemiology as well as evolution of virulence, in a susceptible host population. Additionally, intra-stadial transmission provides an increased risk of tick-borne pathogen transmission to humans and domestic animals during slaughter and game hunting.
Peri-implant mucosa is composed of 2 compartments: a marginal junctional epithelium and a zone of connective tissue attachment. Both structures consist mainly of collagen. Lathyrism is characterized by defective collagen synthesis due to inhibition of lysyl oxidase, an enzyme that is essential for interfibrillar collagen cross-linking. The lathyritic agent beta- aminoproprionitrile (ß-APN) is considered a suitable agent to disrupt the connective tissue metabolism. Therefore, the purpose of this study was to assess the effect of defective connective tissue metabolism on epithelial implant interface by using ß-APN created chronic lathyrism in the canine model. Two 1-year-old male dogs were included in this study. A ß-APN dosage of 5 mg/0.4 mL/volume 100 g/body weight was given to the test dog for 10 months, until lathyritic symptoms developed. After this, the mandibular premolar teeth (p2, p3, p4) of both dogs were atraumatically extracted, and the investigators waited 3 months before implants were placed. In the test dog, 3 implants were placed in the left mandible, and 2 implants were placed in the right mandible. In the control dog, 2 implants were placed in the left mandibular premolar site. The dogs were sacrificed 10 months after healing. Periimplant tissues obtained from the dogs were examined histomorphologically and histopathologically. Bone to implant contact (BIC) values and bone volumes (BV) were lower in the lathyritic group compared to the control group; however, no statistical significance was found. Significant histologic and histomorphometric changes were observed in periimplant bone, connective tissue, and peri-implant mucosal width between test and control implants. Defective collagen metabolism such as lathyrism may negatively influence the interface between implant and surrounding soft tissue attachment.
Sandwich structures with folded cores are regarded as a promising alternative to conventional honeycomb sandwich structures in the aerospace industry. This paper presents a parametric study on the mechanical properties of a variety of Miura-based folded core models virtually tested in quasi-static compression, shear and bending using the finite element method. It is found that the folded core models with curved fold lines exhibit the best mechanical performances in compression and shear while the multiple layered models outperform the other folded core models in bending. Furthermore, the folded core models are compared to a honeycomb core model with the same density and height. In this case, it is shown that the honeycomb core has the best performance in compression while the folded cores have comparable or even better performances in the shear and bending cases. The virtual test results reported in this paper can provide researchers with a general guideline to design the most suitable folded core structure for certain applications.
Anahtar Kelimeler :
sbtmr, miura-based folded core, finite element method, sandwich structure, quasi-static test
The relationship between nitric oxide synthase (NOS) immunocytochemistry and NADPH-diaphorase (NADPH-d) histochemistry was investigated in the anterior and posterior pituitary of ovariectomized rats. NADPH-d activity was present throughout the posterior pituitary but could not be detected in the anterior pituitary. By contrast, an antibody raised against whole recombinant rat neuronal NOS revealed strongly NOS-immunoreactive gonadotrophs and folliculo-stellate cells scattered throughout the anterior pituitary in addition to immunoreactive fibres in the posterior pituitary. The study demonstrates that NADPH-d histochemistry is not always coincident with NOS and provides evidence for an as yet uncharacterized subtype of NOS in the rat anterior pituitary.
Origami geometric design is fundamental to many engineering applications of origami structures. This paper presents a new method for the design of three-dimensional (3D) origami structures suitable for engineering use. Using input point sets specified, respectively, in the x−z and y−z planes of a Cartesian coordinate system, the proposed method generates the coordinates of the vertices of a folded origami structure, whose fold lines are then defined by straight line segments each connecting two adjacent vertices. It is mathematically guaranteed that the origami structures obtained by this method are developable. Moreover, an algorithm to simulate the unfolding process from designed 3D configurations to planar crease patterns is provided. The validity and versatility of the proposed method are demonstrated through several numerical examples ranging from Miura-Ori to cylinder and curved-crease designs. Furthermore, it is shown that the proposed method can be used to design origami structures to support two given surfaces.
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
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
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
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
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 email@example.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
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 firstname.lastname@example.orgBackground: 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
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
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