MicroRNA-23b inhibits cell viability and migration but promotes apoptosis in non-small cell lung cancer cells in vitro

Background: Lung cancer is a major public health problem worldwide and currently its effective therapies are still imperfect. MicroRNA-23b (miR-23b) was reported to modulate various cancer pathological conditions. Our study was aimed to reveal the potential effect of miR-23b on non-small cell lung cancer (NSCLC) cells and its possible mechanism. Methods: NSCLC cells line A549 were transfected with miR-23b mimic, miR-23b inhibitor or control, the miR-23b expression was monitored by quantitativepolymerase chain reaction (qPCR). The cell viability, migration and apoptosis of A549 cells were respectively measured by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyltetrazolium bromide (MTT), modified two-chamber migration assay, and flow cytometry. Western blot was used to detect the phosphorylation levels of phosphatidylinositol 3-kinase (PI3K), AKT (Protein Kinase B) andglycogen synthase kinase-3 beta (GSK3 beta) in transfected cells. Results: In A549 cells, miR-23b was effectively overexpressed and suppressed (P < 0.001). We observed that miR-23b overexpression significantly suppressed A549 cells viability (P < 0.05 or P < 0.01) and migration (P < 0.001), but enhanced apoptosis (P < 0.001). In contrast, miR-23b suppression displayed the contrary results (P < 0.05, P < 0.01 or P < 0.001). In addition, we found that miR-23b overexpression downregulated the phosphorylation levels of PI3K, AKT, and GSK3 beta in A549 cells, whereas miR-23b suppression could upregulate them. Conclusion: MiR-23b overexpression suppressed A549 cells viability and migration, but enhanced apoptosis through the PI3K/AKT/GSK3 beta pathway. Overexpression of miR-23b has potential as a novel therapeutic strategy in NSCLC treatment.