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

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.

microRNA-184 in the landscape of human malignancies: a review to roles and clinical significance

“…DLX1 is a protein that binds to β-catenin and enhances viability and migratory capacities of cancer cells through activation of the β-catenin/TCF signaling pathway [116]. miR-184 is reported with downregulated expression in PC tissues and cell lines (C4-2, PC-3, Du145, and LNCaP) relative to normal prostate tissues and RWPE-2 cell lines, respectively [117]. miR-184 overexpression suppressed the growth and malignant activities of PC cells, while exogenous expression of DLX1 showed reverse impact.…”

In silico investigation of the role of miRNAs in a possible developmental origin of prostate cancer in F1 and F2 offspring of mothers exposed to a phthalate mixture

“…27 In addition, epigenetic mechanisms modulated by environmental factors may be the key to establishing the relationship between the effects of modulation with different diseases. 28 The mir-184 is thought to be a tumor suppressor and its up-regulation can inhibit migration and invasion of prostate cancer cells by decreasing mRNA expression of targets as DLX1, 29 which stimulates cancer cell viability and migration through β-catenin activation. 29,30 The upregulation of rno-miR-184 has been pointed to as a great biomarker of benign prostatic hyperplasia in rats.…”

“…28 The mir-184 is thought to be a tumor suppressor and its up-regulation can inhibit migration and invasion of prostate cancer cells by decreasing mRNA expression of targets as DLX1, 29 which stimulates cancer cell viability and migration through β-catenin activation. 29,30 The upregulation of rno-miR-184 has been pointed to as a great biomarker of benign prostatic hyperplasia in rats. 31 In humans, hsa-miR-184 expression was identified in prostate cancer with high aggressivity.…”