Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

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

Xiuqing Li¹, Hui Zhang², Tao Cui³, Youshan Wu¹, Shougang Wang⁴

¹Department of Gastroenterology and Hepatology, Affiliated Lianyungang Oriental Hospital of Xuzhou Medical University, Lianyungang City 222042; ²Department of Gastroenterology and Hepatology, The Second Hospital of Lianyungang, Lianyungang City 222023; ³Department of Gastroenterology; ⁴Office of Academic Affairs, Affiliated Hospital of Beihua University, Jilin City, Jilin Province 132011, China.

For correspondence:- Shougang Wang Email: wangshougang97@163.com Tel:+8643262166044

Accepted: 29 June 2021 Published: 29 July 2021

Citation: Li X, Zhang H, Cui T, Wu Y, Wang S. MiR-143-5p inhibits proliferation, invasion, and epithelial to mesenchymal transition of colorectal cancer cells by downregulation of HMGA2. Trop J Pharm Res 2021; 20(7):1337-1343 doi: 10.4314/tjpr.v20i7.3

© 2021 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

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.

Keywords: MiR-143-5p, High-mobility Group AT-Hook 2, HMGA2, Colorectal cancer, Epithelial-mesenchymal transition, EMT, Cell proliferation