Regulatory role of the miR-142-3p/ axis in modulating autophagy in non-small cell lung cancer.

Background: With its diverse genetic foundation and heterogeneous nature, non-small cell lung cancer (NSCLC) needs a better comprehension of prognostic evaluation and efficient treatment targeting.

Methods: Bioinformatics analysis was performed of The Cancer Genome Atlas (TCGA)-NSCLC and GSE68571 dataset. Overlapping differentially expressed genes (DEGs) were used for functional enrichment analysis and constructing the protein-protein interaction (PPI) network. In addition, key prognostic genes were identified through prognostic risk models, and their expression levels were verified. The phenotypic effects of cell division cycle 25C () regulation on NSCLC cell lines were assessed by experiments using various techniques such as flow cytometry, Transwell, and colony formation. Protein levels related to autophagy and apoptosis were assessed, specifically examining the impact of autophagy inhibition [3-methyladenine (3-MA)] and the miR-142-3p/ axis on this regulatory system.

Results: was identified as a key prognostic marker in NSCLC, showing high expression in tumor samples. experiments showed that knockdown markedly reduced the capacity of cells to proliferate, migrate, invade, trigger apoptosis, and initiate cell cycle arrest. and miR-142-3p displayed a reciprocal regulatory relationship. reversed the inhibitory impacts of miR-142-3p on NSCLC cell cycle proliferation and progression. The synergy of miR-142-3p inhibition, silencing, and 3-MA treatment was shown to regulate NSCLC cell processes including proliferation, apoptosis, and autophagy.

Conclusions: MiR-142-3p emerged as a key player in governing autophagy and apoptosis by directly targeting expression. This emphasizes the pivotal role of the miR-142-3p/ axis as a critical regulatory pathway in NSCLC.