【Abstract】Objective To construct coinfected Bad overexpression and shAkt2 lentiviral vector systems NSCLC cell lines and explore the molecular crosstalk of Akt2 and BAD in NSCLC. Methods Bad overexpression lentivirus expressing vector infected shAkt2 NSCLC cells. After selection of Puromycin resistance cells, protein expression levels of Bad were determined western blot, respectively. The cells were divided into NSCLC normal control groups, Bad overexpression cells, shAkt2 cells, Bad+shAkt2 cells and their negative control (NC). Cells were characterized in vivo using apoptosis analysis and cell invasion assay. Expression levels of caspase9, cytoc, BCL2 and BCLXLwere determined by westernblot. Tumorigenicities of H1299 and SPCA1 were assessed using nude mouse xenograft models in vivo.Results After coinfection of Bad+shAkt2 lentiviral vector systems in NSCLC cells, apoptosis were more significantly promoted than that of control and single lentiviral group in vitro and vivo (P＜005). Bad+shAkt2 and shAkt2 groups showed lower caspase9 expression (P＜005). BAD, Bad+shAkt2 and shAkt2 groups showed higher cytoc expression levels.Conclusion Silencing Akt2 combined with Bad overexpression have synergistic effect in promoting NSCLC cell apoptosis, inhibition of NSCLC cells tumorigenic ability. Targeted silencing of Akt2 combined with Bad overexpression can significantly increase the expression of cytoc, downregulating the expression of caspase9, Akt2/Bad Signaling Passway could be involved in the molecular mechanim of NSCLC via promoting apoptosis.