Zhen-min Sun1, Yan Xiao, Li-li Ren, Xiao-bo Lei, Jian-wei Wang. 1. State Key Laboratory of Molecular Virology and Genetic Engineering, Institute of Pathogen Biology, Peking Union Medical College & Chinese Academy of Medical Sciences, Beijing 100730, China
Abstract
OBJECTIVE: To explore the molecular mechanism of apoptosis induced by enterovirus 71 (EV71) infection. METHODS: The effects of EV71 on Rhabdomyosarcoma (RD) cell viability were detected by CCK8 assay. EV71-induced apoptosis on RD cells were detected by Hoechst 33342 staining and Western blot targeting Caspase 3, 8 and PARP. Bax conformational change was detected by immunoprecipitation with Bax 6A7 antibody. RESULTS: EV71 decreased the viability of RD cells and induces the activation of Caspase 3, 8 and PARP. Bax expression increases in RD cells after EV71 infection, and Bax conformational change also can be detected after EV71 infection. CONCLUSION: Our study reveals that EV71 induces Caspase-dependent apoptosis by Bax conformational change.
OBJECTIVE: To explore the molecular mechanism of apoptosis induced by enterovirus 71 (EV71) infection. METHODS: The effects of EV71 on Rhabdomyosarcoma (RD) cell viability were detected by CCK8 assay. EV71-induced apoptosis on RD cells were detected by Hoechst 33342 staining and Western blot targeting Caspase 3, 8 and PARP. Bax conformational change was detected by immunoprecipitation with Bax 6A7 antibody. RESULTS: EV71 decreased the viability of RD cells and induces the activation of Caspase 3, 8 and PARP. Bax expression increases in RD cells after EV71 infection, and Bax conformational change also can be detected after EV71 infection. CONCLUSION: Our study reveals that EV71 induces Caspase-dependent apoptosis by Bax conformational change.