LncRNA PVT1 regulates growth, migration, and invasion of bladder cancer by miR-31/ CDK1.

Abstract

The aim of our study was to validate the sway oflong 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). 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 byquantitative 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. 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. 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.