Beclinl enhances cisplatin-induced apoptosis via Bcl-2-modulated autophagy in laryngeal carcinoma cells Hep-2

To investigate the role of Beclinl in cisplatin-induced apoptosis in laryngeal carcinoma cells Hep-2 and to explore the potential mechanism. We up-regulated Beclinl expression in Hep-2 cells. The survival rate and apoptotic rate were evaluated by WITT and flow cytometry (ECM). The Beclinl overexpression group and the control group were treated with cisplatin for 24 hours. The proliferation and cell apoptosis of laryngeal cancer cell lines were evaluated. The mitochondrial membrane potentials were detected by DiOC6(3). Activities of Caspase-8/9/3 and convention of microtuhule-associated protein one light chain 3 (LC3) were detected by western blot. The effect of Bcl-2 overexpression on increased cisplatin-sensitivity and autophagy induced by Beclinl was investigated using Bc1-2 cDNA transfection. Expression of Beclinl in Hep-2 cells was meaningfully enhanced by transfection, and the proliferation and the apoptosis were not considerably affected. By cisplatin treatment, the Beclinl overexpression group showed lower survival rate and higher apoptotic rate than the control group (p<0.05). Decrease of mitochondria membrane potential and increase of activities of Caspase-8, Caspase-9 and Caspase-3 were detected. Beclinl overexpression increase the convention of LC3, especially after the cisplatin treatment. Overexpression of Bcl-2 decreased the cisplatin-induced apoptosis and inhibited Beclinl-induced autophagy. In conclusion, Beclinl enhances cisplatin-induced apoptosis in laryngeal carcinoma cells Hep-2 via Bcl-2 modulated autophagy.