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

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 BEAS2B 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.