Overexpression of cyclin L2 induces apoptosis and cell-cycle arrest in human lung cancer cells

Background Uncontrolled cell division is one of the hallmarks of tumor growth.Researches have been focused onnumerous molecules involved in this process.Cyclins are critical regulatory proteins of cell cycle progression and/ortranscription.The present study aimed to investigate the anti-proliferative effect of cyclin L2,and to define its growthregulatory mechanisms using human lung adenocarcinoma cell line A549.Methods Human cyclin L2 was transfected into human lung adenocarcinoma cells (A549 cell),and was expressed in amammalian expression vector pcDNA3.1.The effects and mechanisms of the cyclin L2 in cell growth,cell cycle analysisand apoptosis were studied by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (Ml-r),flow cytometry orWestern blot,respectively.Results Overexpression of cyclin L2 inhibited the growth of A549 cells.Cell cycle analysis in cells transfected withpCCNL2 revealed an increment in proportion in G0/G1 phase ((68.07±4.2)%) in contrast to (60.39±2.82)% of the cellstransfected with mock vector.Apoptosis occurred in (7.25±0.98)% cells transfected with pCCNL2,as compared with(1.25±0.21)% of the mock vector control group.Cyclin L2-induced-G0/G1 arrest and apoptosis involved upregulation ofcaspase-3 and downregulation of Bcl-2 and survivin.Conclusion The results indicate that overexpression of cyclin L2 protein may promote efficient growth inhibition ofhuman lung adenocarcinoma ceils by inducing G0/G1 cell cycle arrest and apoptosis.