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.