MiR-143-5p inhibits proliferation, invasion, and epithelial to mesenchymal transition of colorectal cancer cells by downregulation of HMGA2

Abstract

Purpose: To investigate the regulatory effect and molecular mechanism of miR-143-5p in colorectal cancer (CRC) progression. Methods: Expression of miR-143-5p in CRC cell lines SW620 and HCT116 was determined by quantitative real-time polymerase chain reaction (qRT-PCR). Stable miR-143-5p overexpression was mediated by lentivirus. The effects of miR-143-5p on proliferation, migration, invasion, and epithelial- mesenchymal transition (EMT) of SW620 and HCT116 cells were assessed by colony formation assay, CCK-8, Transwell assay, wound healing assay, and western blot. Target prediction was performed for miR-143-5p, and a dual luciferase assay was used to verify the targeting relationship. Results: Compared to CRC cells transfected with negative controls, cell proliferation, migration and invasion, and EMT were inhibited in miR-143-5p-overexpressing cells. Expression of HMGA2 (high- mobility Group AT-Hook 2), a target gene of miR-143-5p, was repressed by miR-143-5p. Rescue experiments confirmed that upregulation of HMGA2 due to mIR-143-5p overexpression reversed inhibition of CRC cell proliferation, invasion and EMT. Conclusion: MiR-143-5p inhibits the malignant progression of CRC by regulating HMGA2 expression and is expected to provide new therapeutic approaches for clinical treatment of CRC.