lncRNA LOC339524 inhibits the proliferation of bladder cancer cells by targeting the miR-875-5p/COPS7A signaling axis

xlomafota13 shared this article with you from Inoreader lncRNA LOC339524 inhibits the proliferation of bladder cancer cells by targeting the miR-875-5p/COPS7A signaling axis Via Experimental and therapeutic medicine Exp Ther Med. 2021 Nov;22(5):1202. doi: 10.3892/etm.2021.10636. Epub 2021 Aug 23. ABSTRACT It has been reported that long non-coding RNAs (lncRNAs) play a crucial role in the progression of various types of cancer. The role of numerous lncRNAs in a variety of cancer types has been investigated. However, the underlying mechanisms of the majority of lncRNAs in bladder cancer (BCa) remain to be elucidated. In the present study, abnormally expressed lncRNAs in BCa and para-carcinoma tissues were identified through screening the Cancer RNA-Seq Nexus database and were validated using reverse transcription-quantitative PCR. It was found that LOC339524 expression levels were markedly downregulated in BCa tissues and cells (J82, T24, UM-UC-3 and 5637). LOC339524 overexpression was revealed to suppress the proliferation of BCa cells. LOC339524 was also discovered to act as a sponge for microRNA (miR)-875-5p, as identified using dual luciferase r eporter assays and biotin pull-down analysis. LOC339524 downregulated the expression of miR-875-5p and knockdown of miR-875-5p expression inhibited the proliferation of bladder cancer cells. In addition, COP9 signalosome subunit 7A (COPS7A) was identified to be the target gene of miR-875-5p and COPS7A expression level was upregulated following LOC339524 overexpression. lncRNA LOC339524 was proposed to function as a competitive endogenous RNA to facilitate the expression of COPS7A by binding to miR-875-5p. In conclusion, the findings of the present study suggested that LOC339524 may inhibit cell proliferation in BCa by targeting the miR-875-5p/COPS7A signaling axis. PMID:34584547 | PMC:PMC8422399 | DOI:10.3892/etm.2021.10636 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.