Effect and mechanism of miR-155 on proliferation of laryngeal squamous cell carcinoma Hep2 cell line

Objective To explore effect and mechanism of microRNA-155 (miR-155) on the proliferation of laryngeal squamous cell carcinoma Hep2 cells.Methods Hepatocellular carcinoma Hep2 cells were transfected with miR-155 NC and miR-155 inhibitor with liposomes.The expression of miR-155 was detected with realtime-PCR.The viability of the cells with different transfection time (12,24,36,48,60,and 72 hours) was detected with Cell Counting Kit-8 (CCK-8) assay.Cell apoptosis and cell cycle were determined with flow cytometry.The expressions of cell cycle protein A1 (cyclinA1),cell cycle protein D1 (cyclinD1),phosphatidylinositol 3 kinase (PI3K)/protein kinase B (AKT),and forkhead box 3a (Foxo3a) signal pathway related proteins were detected with Western blot.Results The expression of miR-155 in the Hep2 cells transfected with miR-155 inhibitor was obviously lower than that in the cells transfected with miR-155 NC (0.34±0.03 vs.1.25±0.10) and the viability of Hep2 cells transfected with miR-155 inhibitor was lower than that of cells with miR-155 NC 24,36,48,60,and 72 hours after the transfection.Compared to those transfected with miR-155 NC,the Hep2 cells transfected with miR-155 inhibitor showed significantly increased apoptotic rate,the cell cycle arrested in G1,significantly down-regulated expressions of cyclinA1,cyclinD1,PI3K and p-AKT,and significantly up-regualated expression of Foxo3a (all P<0.01).Conclusion miR-155 inhibitor could affect the proliferation and apoptosis of Hep2 cells and the effects may relate to the regulation of PI3K/AKT/Foxo3a signal pathway.