MiR-221 affects the proliferation and apoptosis of laryngeal cancer cells through the PI3K/AKT signaling pathway

OBJECTIVE To investigate the effect of MiR-221 on proliferation and apoptosis of laryngeal carcinoma cells through the PI3K/AKT signaling pathway. MATERIALS AND METHODS LipofectamineTM 2000 liposomes were used to transfer MiR-221 analogue, MiR-221 NC into Hep-2 cells of laryngeal carcinoma. Real-time fluorescence quantitative polymerase chain reaction (PCR) method was used to detect the expression of MiR-221, MTT method was used to detect the proliferation of cells, flow cytometry was used to detect cell cycle, Western blotting was used to detect the expression of apoptosis proteinase-1 (Apaf-1) and cyclin-dependent kinase (CDK1, CDK2) protein and the activation of phosphatidylinositol 3 kinase (PI3K)/protein kinase B (AKT). RESULTS Compared with MiR-221 NC group, the expression of MiR-221 in MiR-221 analogue group was up-regulated (p<0.01), the cell proliferation rate was decreased (p<0.01), the cell cycle was stagnated in the G1 phase (p<0.01), the expression levels of Cyclin A, CDK1, CDK2, PI3K, and p-AKT were significantly down-regulated (p<0.01), and the expression levels of Bax and Apaf-1 were significantly up-regulated (p<0.01). CONCLUSIONS MiR-221 analogues can significantly inhibit the proliferation and induce apoptosis of Hep-2 cells in laryngeal cancer, and this is achieved by blocking the PI3K/AKT signaling pathway, which also indicates that MiR-221 affects the proliferation and apoptosis of laryngeal cancer cells through the PI3K/AKT signaling pathway.