MicroRNA‑628‑5p inhibits cell proliferation and induces apoptosis in colorectal cancer through downregulating CCND1 expression levels
Affiliations: Department of General Surgery, The First Affiliated Hospital of Hebei North University, Zhangjiakou, Hebei 075061, P.R. China
- Published online on: January 16, 2020 https://doi.org/10.3892/mmr.2020.10945
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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.