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.

<p>Cytochrome C Oxidase Assembly Factor 1 Homolog Predicts Poor Prognosis and Promotes Cell Proliferation in Colorectal Cancer by Regulating PI3K/AKT Signaling</p>

“… 26 Downregulation of CCND1 may repress the progression of CRC. 27 mTOR is an atypical serine/threonine protein kinase that belongs to the PI3K family and serves as a downstream effector of the PI3K/Akt pathway signaling to regulate cellular functions. 28 The activation of mTOR accelerates cell growth and proliferation, and the inhibition of mTOR limits cell growth.…”

Downregulated miR-150-5p in the Tissue of Nasopharyngeal Carcinoma

“…MiR-584 targets CCND1 to inhibit invasion and proliferation of pancreatic carcinoma [39]. In colorectal carcinoma, miR- 628-5p can downregulate CCND1 expression to induce apoptosis and restrain cell proliferation [40]. In ovarian cancer, the inhibition of CCND1 expression by cisplatin can reduce cell proliferation and increase cell apoptosis [41].…”

Cytokines regulate stemness of mesenchymal stem cells via miR‐628‐5p during periodontal regeneration

“…For example, during human MSC (hMSC)‐induced osteogenesis miR‐96, miR‐124, miR‐199a, 16 and miR‐299‐5p 17 are upregulated, whereas miR‐101‐3p, 10 miR‐148a, 18 miR‐424, 18 and miR‐204 19 are downregulated. Another miRNA, miR‐628‐5p, regulates cell functions and apoptosis 20,21 and, may therefore, play an important role in periodontal tissue differentiation 22 . Predicted targets for miR‐628‐5p include CCND1 , IFI44L , and FRFR 20,21,23 .…”

“…Another miRNA, miR‐628‐5p, regulates cell functions and apoptosis 20,21 and, may therefore, play an important role in periodontal tissue differentiation 22 . Predicted targets for miR‐628‐5p include CCND1 , IFI44L , and FRFR 20,21,23 . While FGFR has been reported to be involved in the regulation of cell differentiation, 7 transcription factors, such as ETV1, SOX11, and GATA6, are known to keep MSCs in an undifferentiated state and to regulate cellular functions 22,24 .…”