Effects of MicroRNA-22 (miR-222) on Non-Small-Cell Lung Carcinoma (NSCLC) Cells Apoptosis and Proliferation Through Protein Kinase B/Mammalian Target of Rapamycin (AKT/mTOR) Signaling Pathway

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Our study investigated miR-222’s effect on NSCLC apoptosis and proliferation. H1650 cells were assigned into NSCLC group, SI group and IN group followed by analysis of Akt-mTOR protein content, cell apoptosis and proliferation, and miR-222 expression by Western blot, Hoechst 33258 fluorescence staining, qRT-PCR, cck-8, and immunohistochemistry miR-222 expression was lowest in IN group and highest in SI group (P < 0.05). The nucleus shrinkage rate in IN group and NSCLC group was significantly higher than that in SI group (P < 0.05) with NSCLC group showed more cells apoptosis than IN group (P < 0.05). The SI group had significantly higher OD value than IN group and NSCLC group (P < 0.05) with NSCLC group having significantly higher OD value than IN group (P < 0.05). The Akt-mTOR and p-Akt/p-mTOR expression was lowest in IN group and highest in SI group (P < 0.05) with lower level in IN group than NSCLC group (P < 0.05). The number of positive Akt-mTOR of H1650 cells was highest in SI group while lowest in IN group (P < 0.05). The decreased miR-222 expression in NSCLC can promote cancer cell apoptosis and inhibit lung cancer development, which may be via down-regulating Akt-mTOR signaling.