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Taken together, the results indicated that miR-767 expression is upregulated in both NSCLC clinical samples and cells. The downregulation of miR-767 can inhibit tumor cell proliferation, migration and invasion, and these effects are further promoted by UTMD-mediated miR-767 inhibition, which indicated the potential of a UTMD-mediated miR-767 inhibition as a novel therapeutic strategy for NSCLC treatment. Copyright © 2020, Spandidos Publications.MicroRNAs (miRNAs) are reported to play a critical role in the regulation of cancer cell proliferation; however, the role of microRNA-25 (miR-25) in pancreatic ductal adenocarcinoma (PDAC) remains unclear. In the present study, the role of miR-25 in PDAC cell proliferation was investigated. Upregulated expression of miR-25 was found in PDAC tissues and cell lines by reverse transcription-quantitative PCR. Cell proliferation was significantly enhanced by overexpression of miR-25 as shown by CCK-8 assay results. Meanwhile, overexpression of miR-25 also promoted G1-to-S phase transition of the cell cycle in Aspc-1 cells via flow cytometry analysis. However downregulation of miR-25 inhibited the tumor cell proliferation and cell cycle transition. Online software was used to predict the target gene for miR-25 and luciferase reporter assay confirmed that Abl interactor 2 (ABI2) was a target of miR-25 via direct binding of its 3' untranslated region with miR-25. Moreover, results of the western blot analysis demonstrated that miR-25 negatively regulated the expression of ABI2 at the protein level. In addition, introduction of ABI2 mRNA into cells overexpressing miR-25 attenuated the carcinogenic effects of miR-25. In conclusion, these findings demonstrate that miR-25 plays an oncogenic role and promotive role in PDAC cell proliferation via targeting of ABI2. Copyright © 2020, Spandidos Publications.Long non-coding RNA gastric cancer associated transcript 3 (GACAT3), is a newly identified non-coding RNA, which has been found to be involved in the tumorigenesis of gastric cancer. However, the biological function of GACAT3 in liver cancer remains unclear. The present study aimed to determine the expression level and function of GACAT3 in liver cancer. The authors cultured liver cancer cells in vitro and GACAT3 was silenced in the cells. Cell proliferation, apoptosis and migration were determined by MTT assay, flow cytometric analysis and transwell assay, respectively. It was demonstrated that GACAT3 was upregulated in liver cancer tissues. The inhibition of GACAT3 decreased the ability of hepatoma cells to proliferate and migrate, and increased apoptosis of the cells. These findings provide the first evidence, to the best of our knowledge, of the exact role of GACAT3 in liver cancer, suggesting GACAT3 as a potential target for liver cancer therapy in the future. Copyright © Dong et al.Indicators for predicting the efficacy of mycophenolate mofetil (MMF) have so far remained elusive. The present study aimed to identify predictive indicators of the efficacy of MMF combined with low-dose prednisone in patients with IgA nephropathy. A total of 598 patients presenting with primary IgA nephropathy at our center were screened. Patients were followed up for 18 months, where the end-point was defined as complete clinical remission. Cox proportional hazards models were performed for analyzing the initial serum creatinine (SCr) concentration to predict incomplete clinical remission. In total, 7 of 71 patients (9.86%) were in complete clinical remission at the final visit. Logistic regression indicated that the hazard ratio (HR) for quartile 4 was significantly higher than the HR for quartile 1 (quartile 4 vs. quartile 1 HR, 2.51; 95% CI, 1.20-5.21; P=0.01). Additional adjustment for the confounding variables, including age, sex, systolic BP, diastolic BP, proteinuria, uric acid, serum triglyceride, hemoglobin, serum albumin, serum total cholesterol and The Oxford classification of the models, did not reduce the HRs for the association between the initial SCr concentration and risk of incomplete clinical remission (quartile 4 vs. quartile 1 HR, 7.27; 95% CI, 1.21-43.63; P=0.03). Each unit increase in the initial SCr concentration was associated with a 67 and 194% increase in the risk of incomplete clinical remission based on model 1 (95% CI, 1.02-2.73; P=0.04) and model 2 (95% CI, 1.01-8.60; P=0.048), respectively. In conclusion, in the present cohort of patients with IgA nephropathy treated with MMF plus low-dose prednisone, the initial SCr concentration was an independent risk factor for incomplete clinical remission. Copyright © 2020, Spandidos Publications.The current study investigated the protective effects of inactivated pseudomonas aeruginosa (IPA) on myocardial ischemia reperfusion injury (MIR/I) and the mechanisms governing this interaction. Left anterior descending coronary artery ligation was performed on rats for 30 min and reperfusion was performed for a subsequent 2 h. Rat hearts were obtained and the myocardial infarction area was determined using nitroblue tetrazolium. Myocardial cell apoptosis was determined using flow cytometry. Malondialdehyde (MDA) content, lactate dehydrogenase (LDH) activity, superoxide dismutase (SOD) activity and catalase (CAT) activities were assayed using the corresponding kits. Additionally, nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase 1 (HO-1) were assayed using western blot and immunofluorescence analysis. When compared with the model group, the results of IPA treatment revealed improved heart function, reduced myocardial infarction area and reduced endothelial cell apoptosis, which led to decreased LDH and MDA levels, and increased SOD and CAT levels in serum, and decreased LDH and MDA levels and increased SOD and CAT in myocardial tissues. Moreover, increased Nrf2 and HO-1 expression levels in the myocardial tissues were also observed at all concentrations of IPA. It was concluded that IPA pretreatment ameliorated MIR/I and reduced endothelial apoptosis and oxidative stress via the Nrf2/HO-1 pathway. Copyright © 2019, Spandidos Publications.Colorectal cancer (CRC) is one of the most lethal tumor types worldwide. Circular RNAs (circRNAs), which are covalent closed loops of RNA, perform vital roles for the proliferation and metastasis of a variety of tumor types. In the present study, the expression, function and molecular mechanisms of action of a novel circRNA, circRNA_101951, were examined in CRC. The expression levels of circRNA_101951 in CRC tissue and cell lines were examined using reverse transcription-quantitative (RT-qPCR). learn more Cell proliferation, the clone formation ability, cell apoptosis, the cell cycle and the cell migratory and invasive abilities were examined using MTT assays, colony formation assays, flow cytometric assays, and cell migration and invasion assays, respectively. The effects of circRNA_101951 on Kinesin II family member 3A (KIF3A) related gene expression were examined using RT-qPCR and western blot assays. The results indicated that circRNA_101951 was increased in CRC tissues and cell lines. The downregulation of circRNA_101951 inhibited cell proliferation and colony formation as well as cell migration and invasion of CRC cell lines. In addition, the downregulation of circRNA_101951 blocked the KIF3A-mediated epithelial-mesenchymal transition (EMT) pathway, which was detected by examining the expression levels of KIF3A and EMT related proteins. In conclusion, the current data revealed that circRNA_101951 may act as a potential biomarker for patients with CRC, and provided a novel insight demonstrating that the suppression of circRNA_101951 may be a potential therapeutic strategy for CRC. Copyright © Li et al.Long noncoding RNAs (lncRNAs) and microRNAs (miRs) serve critical roles in various cellular processes and can be used as noninvasive biomarkers in human diseases. The present study aimed to investigate the effects of lncRNA plasmacytoma variant translocation 1 (PVT1) and miR-190a-5p on vascular endothelial cell (EC) proliferation and assess their clinical value in the diagnosis of chronic heart failure (CHF). The expression of PVT1 and miR-190a-5p was investigated using reverse transcription-quantitative PCR. The interaction between PVT1 and miR-190a-5p was confirmed using a luciferase reporter assay. A Cell Counting Kit-8 assay was performed to examine EC proliferation. A receiver operating characteristic (ROC) curve was plotted to evaluate the diagnostic value of PVT1 and miR-190a-5p. PVT1 directly decreased the expression of miR-190a-5p in ECs. Overexpression of miR-190a-5p in ECs led to inhibited cell proliferation and miR-190a-5p antagonized the promotive effect of PVT1 on EC proliferation. Serum expression of PVT1 increased, while serum expression of miR-190a-5p decreased in patients with CHF compared with healthy controls (all P less then 0.001). The ROC curves indicated that PVT1 and miR-190a-5p were two diagnostic biomarkers of CHF, and the combination of PVT1 and miR-190a-5p showed better diagnostic accuracy compared with using PVT1 or miR-190-5p alone. In conclusion, the present study demonstrated that PVT1 promoted EC proliferation by directly suppressing miR-190a-5p. Circulating PVT1 and miR-190a-5p are possible two candidate diagnostic biomarkers of CHF, and the combined detection of the two indicators may provide a novel approach for CHF diagnosis. Copyright © Sun et al.Tongue squamous cell carcinoma (TSCC) is a common malignancy in oral cancer with a high mortality and morbidity. The ectodysplasin-A receptor-associated adaptor protein (EDARADD) is a death domain-containing adaptor protein that interacts with the TNF family ligand ectodysplasin A receptor. It is known that EDARADD has an effect on the development of ectodermal derivative tissues, such as hair and teeth. EDARADD expression is also associated with the development of melanoma. However, the role of EDARADD in TSCC remains unknown. The aim of the present investigation was to explore whether EDARADD plays a role in the biological function of TSCC. Immunohistochemistry was used to measure the expression of EDARADD in TSCC tissues and adjacent normal tissue. EDARADD was knocked down in a TSCC cell line in vitro using a specific lentivirus. The expression level of the EDARADD gene and the efficacy of gene knockdown were evaluated by reverse transcription-quantitative PCR, while EDARADD protein expression and the expression levels of Bcl-2, MYC and NF-κBp65 were determined by western blotting. Additionally, MTT assays, colony formation assays and apoptosis assays were carried out to examine the effect of EDARADD knockdown on the TSCC cells. A previous study showed that the majority of the TSCC tissues that were tested had high EDARADD expression. The expression of EDARADD both at mRNA and protein levels was significantly lower (P less then 0.01) after the gene was knocked down in the CAL27 cells compared with the level in control cells. Downregulation of EDARADD expression inhibited colony formation and proliferation and induced apoptosis of CAL27 cells when compared to control cells (P less then 0.01). Taken together, these results suggested that EDARADD may be actively involved in the progression of TSCC and that EDARADD may be a novel therapeutic target for the treatment of TSCC. Copyright © Li et al.