Shikonin Induces Oxidative Damage and Promotes Cell Senescence in Lung Cancer Cells through p53/p21WAF Signaling Pathway
Department of Oncology, The Third People's Hospital of Chengdu, Chengdu, Sichuan Province 610031, China
Jun Zhang, Department of Oncology, The Third People's Hospital of Chengdu, Chengdu, Sichuan Province 610031, China, E-mail: firstname.lastname@example.org
To investigate the effect of shikonin on the oxidative damage of lung cancer cells and promotes cell senescence through p53/p21Waf signaling pathway. The lung adenocarcinoma A549 cells were cultured and made into cell suspension. The lung adenocarcinoma A549 cells were cultured for 12 h, 24 h and 48 h respectively with different concentrations of shikonin (0 μm, 2 μm and 4 μm) and the activity of lung adenocarcinoma A549 cells was detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide method. The cell cycle of each group was measured by flow cytometry after 48 h of action of shikonin. The aging of each group of cells was determined by beta-galactosidase staining after 48 h of action of shikonin. The reactive oxygen species content in each group was determined by flow cytometry 48 h after the action of shikonin. The expression levels of cyclin D1, demethylase KDM2B, deoxyribonucleic acid damage marker protein p-H2AX, p53 and p21WAF were measured by Western blot. With the increase of shikonin concentration, the cell activity and the expression levels of cyclin D1 and KDM2B were significantly decreased, the proportion of resting phase/intermediate phase cells and senescent cells were significantly increased, the level of reactive oxygen species and the expression levels of p-H2AX, p53 and p21WAF were significantly increased (p<0.05). Shikonin can inhibit cell activity, induce oxidative damage and promote cell senescence, which may be achieved by activating p53/p21WAF signaling pathway.