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

摘要

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-a 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.