| ObjectiveTumor cell apoptosis resistance is a major problem that the clinical drug treatment has limitations.CD317 as a new tumor related antigen is overexpressed in human cancers and its roles remain controversial,and it happens in tumor development especially in the role of tumor cell apoptosis that is unknown.The topic throughCD317 gene silencing to discuss its role in tumor cell apoptosis,can make a clear definition of the molecular mechanism of tumor cell apoptosis,and then provides a new perspective to the discovery of tumor therapeutic targets.MethodsIn vitro,we examined the effect of knockdown of CD317 in three different human female malignant cells on tumor apoptosis.To evaluate its functional role in cancer apoptosis,CD317 overexpressing cells were transfected with hCD317 si RNA.Reduction in CD317 expression was confirmed both by QPCR and Western Blotting.As measured by FACS detection the ratio of apoptosis,a decline in CD317 levels detectably enhanced apoptotic cell death induced by serum-starvation.ResultsIn our research,CD317 attenuated cell apoptosis ratio in FBS-free condition.Anti-apoptotic effects of CD317 did not depend on autophagy flow.CD317 knockdown did not affect LC3 and caspase activation,but enhanced the nuclear translocation of apoptosis-induced factor(AIF).The inhibition of CD317 on the apoptosis of tumor cell induced by serum starvation,which mechanism may be through the mitochondrial pathway.ConclusionsCD317 contributes to the resistance to apoptosis of tumor cells in vitro via the mitochondrial pathway.Thus,CD317 may be as a potential target for the development of new therapeutics for CD317-dependent cancers. |