MicroRNA‑628‑5p inhibits cell proliferation and induces apoptosis in colorectal cancer through downregulating CCND1 expression levels.

Abstract

MicroRNA (miR)-628-5p serves as an antitumor gene in a variety of cancers; however, the role of miR-628-5p in colorectal cancer remains largely unclear. The purpose of this study was to investigate the role and mechanism of miR-628-5p in colorectal cancer. Reverse transcription-quantitative PCR (RT-qPCR), colony formation assays and flow cytometric analysis were used to determine the expression levels of miR-628-5p in colorectal cancer tissues and cell lines, and the proliferative ability of colorectal cancer cells. TargetScan version 7.2 and dual-luciferase reporter assay were performed to predict and confirm miR-628-5p target genes. The expression levels of cyclin D1 (CCND1) and related genes were determined using RT-qPCR or/and western blotting analysis. miR-628-5p mimics and CCND1 plasmids were used to overexpress miR-628-5p and CCND1; it was demonstrated that the expression levels of miR-628-5p were significantly downregulated in colorectal cancer tissues and cell lines. miR-628-5p mimic-transfected cells inhibited the proliferation and induced apoptosis of HT-29 cells. CCND1, a downstream effector of miR-628-5p, promoted the proliferation and suppressed apoptosis of HT-29 cells, and the effects were reversed by miR-628-5p mimics. In conclusion, the present study suggested that colorectal cancer progression may be regulated through the miR-628-5p/CCND1 axis, and miR-628-5p could be used as a potential diagnostic and prognostic biomarker for colorectal cancer.