MicroRNA‐140‐3p inhibits proliferation and promotes apoptosis in non‐small cell lung cancer by targeting MDIG

Abstract Background MicroRNAs (miRNAs) are associated with cancer progression. MiR‐140‐3p is a tumor suppressor. Nevertheless, its function in non‐small cell lung cancer (NSCLC) is unclear. Methods MiR‐140‐3p expression in NSCLC clinical specimens was examined using the TCGA database and real‐time PCR. NSCLC cell proliferation and apoptosis were investigated after the miRNA overexpression. Then, mineral dust‐induced gene (MDIG) levels in NSCLC clinical specimens were monitored by real‐time PCR and western blotting. Bioinformatics predicated the binding of miR‐140‐3p to MDIG, and their relationship was validated by luciferase reporter assay. The miR‐140‐3p/MDIG axis was further validated through rescue experiments. The involvement of STAT3 signaling in the actions of miR‐140‐3p/MDIG axis was investigated. Results MiR‐140‐3p was decreased in NSCLC tissues and negatively correlated with MDIG expression. Additionally, it was also lower in high‐grade specimens than in low‐grade ones. MiR‐140‐3p restrained cell proliferation, facilitated apoptosis, and inhibited STAT3 signaling in NSCLC. Interestingly, MDIG was a target of this miRNA. Furthermore, MDIG upregulation abolished miR‐140‐3p's effect on cell proliferation, apoptosis, and STAT3 pathway in NSCLC cells. Conclusion MiR‐140‐3p restrained NSCLC development through the regulation of the STAT3 pathway by targeting MDIG. This axis may be a promising target for NSCLC treatment.