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.
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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