miR-184 delays cell proliferation, migration and invasion in prostate cancer by directly suppressing DLX1

xlomafota13 shared this article with you from Inoreader miR-184 delays cell proliferation, migration and invasion in prostate cancer by directly suppressing DLX1 Via Experimental and therapeutic medicine Exp Ther Med. 2021 Oct;22(4):1163. doi: 10.3892/etm.2021.10597. Epub 2021 Aug 11. ABSTRACT A number of previous studies have reported that dysregulated miR-184 expression is associated with the development of cancer. The aim of the present study was to investigate the role of miR-184 in prostate cancer (PC) and the mechanism underlying its effects. Data from human tumor tissue samples were collected from The CEancer Genome Atlas to determine the expression levels of miR-184 and DLX1. The miR-184 mimic and pcDNA3.1-DLX1 plasmid were utilized to induce overexpression of miR-184 and DLX1 in Du145 cells, respectively. Cell Counting Kit-8, wound healing and Transwell assays were performed to examine the effects of miR-184 on the aggressiveness of PC cells. Dual-luciferase reporter gene assay was used to investigate the association between miR-184 and DLX1, and reverse transcription-quantitative PCR and western blot analyses were utilized to determine the mRNA and protein levels. miR-184 expression was found to be downregulated whereas DLX1 was upregulated in PC tissues compared with normal prostate tissues. Cell propagation, migration and invasion were all inhibited by miR-184 upregulation in Du145 cells. Dual luciferase reporter assay confirmed the association between miR-184 and DLX1. The inhibitory effect of miR-184 mimic on cell behaviors was reversed by upregulation of DLX1. These findings suggest that miR-184 plays a beneficial role in suppressing the tumorigenesis of PC by directly targeting DLX1, and it may represent a potential therapeutic strategy for PC. PMID:34504608 | PMC:PMC8393589 | DOI:10.3892/etm.2021.10597 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.