MicroRNA‑21 increases cell viability and suppresses cellular apoptosis in non‑small cell lung cancer by regulating the PI3K/Akt signaling pathway.

MicroRNA (miRNA/miR), a type of non‑coding RNA molecule, is able to inhibit the expression of target genes at multiple stagess. There are 800‑1,000 known miRNAs in the human genome, which serve important roles in cell proliferation, differentiation, apoptosis and migration. Previous studies have demonstrated that the expression of miR‑21 is upregulated in numerous types of malignant tumor, and that miR‑21 participates in the occurrence and development of tumors via complex regulatory mechanisms. The present study aimed to investigate the association between miR‑21 expression, cell viability and apoptosis in a lung cancer cell line, and to elucidate the potential mechanisms. miR‑21 or small interfering RNA against miR‑21 were transfected into A549 non‑small cell lung cancer cells. The mRNA expression of miR‑21 was confirmed. Cell viability and apoptosis were examined using MTT and flow cytometric assays, respectively. The expression of certain apoptosis‑associated proteins was detected by western blotting. The results of the present study demonstrated that miR‑21 was able to increase the proliferation of A549 cells by inhibiting cellular apoptosis. miR‑21 inhibited apoptosis by modulating the activation of the phosphatidylinositol 3‑kinase/Rac‑α serine/threonine protein kinase (Akt) pathway in A549 cells. Correspondingly, inhibition of Akt decreased the apoptosis of A549 cells in miR‑21 siRNA‑treated cells. Therefore, the results of the present study demonstrated that miR‑21 increased cell viability by inhibiting apoptosis, through regulation of Akt activation. The present study demonstrated that miR‑21 may be involved in the progression of lung cancer and may be a novel therapeutic target for the disease.