Background: This experimental design was based on lncRNA LINC01194 to explore the pathogenesis of NSCLC. Methods: RT-qPCR was used to detect the expression of lncRNA LINC01194 and miR-486-5p in NSCLC tissues and cell lines. CCK-8, colony formation, and transwell assays were used to examine the effects of lncRNA LINC01194 and miR-486-5p on NSCLC cell proliferation and migration invasiveness. For target gene prediction and screening, luciferase reporter assays were used to verify downstream target genes for lncRNA LINC01194 and miR-486-5p. The protein expression of CDK4 was detected using Western blotting. The tumor changes in mice were detected by in vivo experiments in nude mice. Results: LncRNA LINC01194 was highly expressed in NSCLC tissues and NSCLC lines (A549, H1299, H460 cells, H1975), and lncRNA LINC01194 significantly promoted cell proliferation and migration of NSCLC cells. MiR-486-5p was identified as a potential target for LINC01194, and miR-486-5p was expressed at a low level in NSCLC tissues and NSCLC lines (A549, H1299, H460 cells, H1975). CDK4 was identified as a potential target for miR-486-5p. LncRNA LINC01194 was able to inhibit miR-486-5p expression and upregulate the expression level of CDK4. Finally, the results of in vivo animal models confirmed that lncRNA LINC01194 promoted NSCLC progression by modulating the miR-486-5p/CDK4 axis. Conclusion: LncRNA LINC01194 promoted the progression of NSCLC by modulating the miR-486-5p/CDK4 axis.
Clear cell renal cell carcinoma (ccRCC) is the most popular kidney cancer in adults. Metabolic shift toward aerobic glycolysis is a fundamental factor for ccRCC therapy. MicroRNAs (miRNAs) are thought to be important regulators in ccRCC development and progression. Phosphoinositide-dependent kinase 1 (PDK1) is required for metabolic activation; however, the role of PDK1-induced glycolytic metabolism regulated by miRNAs is unclear in ccRCC. So, the purpose of the current study is to elucidate the underlying mechanism in ccRCC cell metabolism mediated by PDK1. Our results revealed that miR-409-3p inhibited glycolysis by regulating PDK1 expression in ccRCC cells. We also found that miR-409-3p was regulated by hypoxia. Our results indicated that PDK1 facilitated ccRCC cell glycolysis, regulated by miR-409-3p in hypoxia.
Objectives: Cellular cardiomyoplasty has been proposed as an alternative strategy for augmenting the function of diseased myocardium. Many data have suggested that mesenchymal stem cells (MSC) may contribute to the healing of dilated cardiomyopathy. We will investigate whether autotransplantation with MSC can treat end-stage heart failure and its mechanism. Methods: Heart failure was created in 15 swines by right ventricular pacing-induced at the rate of 230 beats per minute for 4 weeks, and 190 beats per minute for another 4 weeks.Bone marrow aspirate was taken from the iliac crest of healthy swines. MSCs were isolated and co-cultured with 5-aza for 24hours. All the swines were divided into three groups: DMEM implantation group (DMEM); MSC implantation group (MSC); cardiomyocyte-like cell implantation group (CSC); The stem cells were injected into coronary artery of the porcines with heart failure under DSA. The ejection fraction (EF), the thickness of left ventricular wall, the diastolic diameter of left ventricle (LVDd) and CO were assessed by echocardiography before and 4 week after implantation.The TNF, TGF were detected with ELISA in the serum;the percentage of apotosis, the concentrtion of collagen and the ratio of collagen I/III were detected in the heart tissues. Results: A part of MSCs induced by 5-aza had morphological changes and 31 % stained positively Troponin I. Compared with that of the control group, LVEDd of implantation groups was smaller 4 weeks after stem cells implantation (P<0.05), whereas EF was increased (P<0.05). The TNF, the concentrtion of collagen and the percentage of apotosis decreased, whereas TGF, the ratio of collagen I/III increased in implantation groups vs control group. Conclusions: The MSCs can differentiate into cardiomyocytes by 5-aza in vitro.Autologous MSC transplantation improves contractibility of heart failure. This improvement might result from BMC-associated myocardial regeneration and neovascularization.This technique may lead to a promising therapy to treat congestive heart failure.
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