Literature DB >> 29725442

miR-486-5p regulates the migration and invasion of colorectal cancer cells through targeting PIK3R1.

Yuhao Zhang1,2, Jun Fu2, Zhijin Zhang2, Huanlong Qin1.   

Abstract

The aim of the present study was to investigate the function of microRNA (miR)-486-5p in colorectal cancer (CRC). Tumor and adjacent normal mucosal tissue samples were collected from patients with CRC. Differences in the expression levels of miR-486-5p between tumor tissues and adjacent normal mucosal tissues were examined using reverse transcription-quantitative polymerase chain reaction. The results demonstrated that miR-486-5p was significantly decreased in tumor tissues compared with the adjacent normal mucosal tissues. Additionally, in vitro experiments were conducted using SW620 CRC cells. The effects of miR-486-5p mimics on cell invasion and cell migration were evaluated using a Transwell assay and a wound-healing assay, respectively. The results demonstrated that treatment with miR-486-5p mimics decreased the migratory and invasive ability of the cells compared with that in the blank and NC control groups, although the underlying molecular mechanisms were not determined. Protein expression levels of phosphatidylinositol 3-kinase regulatory subunit 1 (PIK3R1), matrix metallopeptidases-2 and -9, and phosphorylated (p)-AKT were examined using western blot analysis. The results demonstrated that the expression levels of these proteins decreased in response to treatment with miR-486-5p mimics in comparison with the blank and NC control groups. Taken together, the findings of the present study indicated that miR-486-5p mimics inhibited the progression of CRC by inhibiting the activation of AKT signaling pathway via targeting PIK3R1. Therefore, miR-486-5p may be a potential target for CRC treatment.

Entities:  

Keywords:  colorectal cancer; microRNA-486-5p; phosphatidylinositol 3-kinase regulatory subunit 1

Year:  2018        PMID: 29725442      PMCID: PMC5920487          DOI: 10.3892/ol.2018.8233

Source DB:  PubMed          Journal:  Oncol Lett        ISSN: 1792-1074            Impact factor:   2.967


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