Purpose: The aim of our study was to validate the sway of long noncoding RNA (lncRNA) plasmacytoma variant translocation 1 (PVT1) on the metabolism and growth of bladder cancer cells by microRNA-31 (miR-31)/cyclin-dependent kinase 1 (CDK1). Methods:The Gene Expression Omnibus database was used for analyzing the differentially expressed lncRNA and messenger RNA (mRNA) in bladder cancer tissues, with the highly expressed lncRNA PVT1 and mRNA CDK1 screened out. The expression level of PVT1 was detected by quantitative reverse-transcription polymerase chain reaction, cell viability by Cell Counting Kit-8 assay, cell proliferation and scratch by 5-bromo-2′-deoxyuridine assay, cell migration and invasion by transwell assays, the expression level of CDK1 by immunohistochemistry and western blot analysis, transcription factor targeting by dual-luciferase assay, and the effect of PVT1 on bladder cancer growth by nude mice tumor formation experiment.Results: LncRNA PVT1 and mRNA CDK1 had a higher expression in bladder cancer cells than that in neighboring tissues. Activity, proliferation, colony formation, migration, and invasion of bladder cancer cell were noticeably reduced by the PVT1 inhibitor than that of control group. PVT1 and CDK1 have binding sites with miR-31.When miR-31 decreased, CDK1 mRNA and protein levels increased in vivo experiments in nude mice. When PVT1 was downregulated, the tumor size was significantly reduced and tumor proliferation was curbed. Immunohistochemistry showed that the positive rate of CDK1 and Ki-67 decreased and the expression of miR-31 increased after PVT1 was inhibited.Conclusions: LncRNA PVT1 was overexpressed in bladder cancer cells, and it was downregulated miR-31 to enhance CDK1 expression and facilitate bladder cancer cells proliferation, migration, and invasion. K E Y W O R D S bladder cancer, cyclin-dependent kinase 1, long noncoding RNA plasmacytoma variant translocation 1, microRNA-31
The levels of IL-32, IL-1, and IFN-γ protein and transcripts in serum and PBMCs from hepatitis B patients were higher than those in healthy volunteers. Similarly, both were higher in PBMCs from healthy volunteers stimulated by HBV in vitro. However, the changes in cytokine levels were not proportional to the viral load.
Background: Diazoxide is a selective mitochondrial-sensitive potassium channel opening agent that has a definite effect on reducing myocardial ischemia/reperfusion injury (MIRI). However, the exact effects of diazoxide postconditioning on the myocardial metabolome remain unclear, which might contribute to the cardioprotective effects of diazoxide postconditioning.Methods: Rat hearts subjected to Langendorff perfusion were randomly assigned to the normal (Nor) group, ischemia/reperfusion (I/R) group, diazoxide (DZ) group and 5-hydroxydecanoic acid + diazoxide (5-HD + DZ) group. The heart rate (HR), left ventricular developed pressure (LVDP), left ventricular end-diastolic pressure (LVEDP), and maximum left ventricular pressure (+dp/dtmax) were recorded. The mitochondrial Flameng scores were analysed according to the ultrastructure of the ventricular myocardial tissue in the electron microscopy images. Rat hearts of each group were used to investigate the possible metabolic changes relevant to MIRI and diazoxide postconditioning.Results: The cardiac function indices in the Nor group were better than those in the other groups at the end point of reperfusion, and the HR, LVDP and +dp/dtmax of the Nor group at T2 were significantly higher than those of the other groups. Diazoxide postconditioning significantly improved cardiac function after ischaemic injury, and the HR, LVDP and +dp/dtmax of the DZ group at T2 were significantly higher than those of the I/R group, which could be abolished by 5-HD. The HR, LVDP and +dp/dtmax of the 5-HD + DZ group at T2 were significantly lower than those of the DZ group. The myocardial tissue in the Nor group was mostly intact, while it exhibited considerable damage in the I/R group. The ultrastructural integrity of the myocardium in the DZ group was higher than that in the I/R and 5-HD + DZ groups. The mitochondrial Flameng score in the Nor group was lower than that in the I/R, DZ and 5-HD + DZ groups. The mitochondrial Flameng score in the DZ group was lower than that in the I/R and 5-HD + DZ groups. Five metabolites, namely, L-glutamic acid, L-threonine, citric acid, succinate, and nicotinic acid, were suggested to be associated with the protective effects of diazoxide postconditioning on MIRI.Conclusion: Diazoxide postconditioning may improve MIRI via certain metabolic changes. This study provides resource data for future studies on metabolism relevant to diazoxide postconditioning and MIRI.
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