Long Noncoding LINC00115 Facilitates Cell Growth and Inhibits Apoptosis by Regulating the miR-4701-5p/P4HB Axis in Bladder Cancer.

Abstract

Bladder cancer (BCa) is a prevalent urogenital malignancy, imposing a significant burden on health-care systems worldwide. Long noncoding RNAs (lncRNAs) are important regulators of carcinogenesis and affect BCa progression. In this study, the influence of lncRNA LINC00115 on malignant behavior of BCa cells were explored. Bioinformatics method was used for prediction of gene expression and downstream molecules of LIN00115. LINC00115 expression level in BCa cells was measured using RT-qPCR. After LINC00115 depletion, the proportion of viable, proliferative, and apoptotic BCa cells were calculated by methyl thiazolyl tetrazolium (MTT) assays, colony formation assays, and TUNEL staining, respectively. FISH was performed to verify the cellular distribution of LINC00115. The interaction between LINC00115 and miR-4701-5p and the binding between miR-4701-5p and P4HB were confirmed using RNA pulldown, RNA immunoprecipitation (RIP), and luciferase reporter assays. Experimental results showed that LINC00115 was highly expressed in BCa cells. The silencing of LINC00115 restrained BCa cell proliferation and stimulated apoptosis. LINC00115 could directly bind to miR-4701-5p and thus initiate P4HB upregulation in BCa cells. P4HB 3'untranslated region could be targeted by miR-4701-5p. Additionally, Amplification of P4HB expression offset the effects of LINC00115 knockdown on BCa cell proliferative and apoptotic behaviors. In conclusion, LINC00115 facilitates BCa cell growth and inhibits apoptosis via interaction with miR-4701-5p and upregulation of P4HB.