Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Regulatory mechanism of lncRNA miR143HG in miR-504 and its effect on proliferation and apoptosis of non-small cell lung cancer cells

Zhe Li , Jinhua Liu, Yingqun Zhu, Qian Cai

Department of Pulmonary and Critical Care Medicine, The Third Hospital of Changsha, Changsha, Hunan 410015, China;

For correspondence:- Zhe Li Email: yumiyin0529@163.com Tel:+8673189668355

Accepted: 26 July 2024 Published: 31 August 2024

Citation: Li Z, Liu J, Zhu Y, Cai Q. Regulatory mechanism of lncRNA miR143HG in miR-504 and its effect on proliferation and apoptosis of non-small cell lung cancer cells. Trop J Pharm Res 2024; 23(8):1231-1237 doi: 10.4314/tjpr.v23i8.1

© 2024 The authors.
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Abstract

Purpose: To investigate the expression and functional role of miR143HG in non-small cell lung cancer (NSCLC), and its effect on human lung adenocarcinoma cell behavior.

Methods: Differential expression of miR143HG between NSCLC tissues and healthy counterparts was identified through bioinformatic analysis. Subsequently, this expression difference in A549 and BEAS-2B cells was validated using quantitative polymerase chain reaction (qPCR). Overexpression of miR143HG in A549 cells was achieved through liposome-mediated transfection, while cell proliferation as well as apoptosis levels were assessed using cell counting kit-8 (CCK-8) assay, flow cytometry, and protein blotting. expression of miR-504 (predicted as a target of miR143HG) was determined. Furthermore, A549 cells that overexpress both miR143HG and miR-504 were generated for comparison with cells overexpressing only miR143HG.

Results: Compared to BEAS-2B cells, A549 cells showed significantly reduced miR143HG and elevated miR-504 levels (p < 0.05). In A549 cells with miR143HG overexpression, cell proliferation and miR-504 expression significantly reduced while pro-apoptotic proteins (BAX, p53) significantly increased (p < 0.05). Simultaneous overexpression of miR143HG and miR-504 in A549 cells counteracted the effect of miR143HG alone, thus enhancing proliferation and diminishing pro-apoptotic protein expression, similar to control.

Conclusion: Downregulation of MiR143HG occurs in human lung adenocarcinoma cells. Upregulation of MiR143HG impedes A549 cell proliferation, promotes apoptosis through pro-apoptotic protein modulation and suppresses miR-504. Co-overexpression of miR143HG and miR-504 reverses these effects, resembling control conditions. Thus, miR143HG exerts its anti-cancer effect in A549 cells by modulating miR-504 and activating p53 pathway.

Keywords: lncRNA miR143HG; Non-small cell lung cancer; Proliferation; Apoptosis