This study was to investigate inhibiting effect of structurally unique Second mitochondria-derived activator of caspase (Smac) in combination with Docetaxel on lung cancer cell line A549. Results showed that the expression of Smac in transfected A549 cells was higher than the control cells both at mRNA level and protein level (P<0.05). Smac over-expression induced a little apoptosis, however, when treated with Docetaxel together, the cells showed a higher apoptosis rate. The apoptosis rate was significantly increased in Smac + Docetaxel group when compared with that in Smac group and Docetaxel group (P<0.05). Cells cloning ability in Smac + Docetaxel group was worse than that of other groups (P<0.05), cell mass formed in relatively small quantities and sparse location. Thus, over-expression of Smac increases the sensitivity of lung cancer A549 cells to Docetaxel treatment, and transfection of Smac to tumor cells might provide a potential therapy modality.
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