Abstract
A series of structurally unique second mitochondria-derived activator of caspases (Smacs) that act as antagonists of the inhibitor of apoptosis proteins (IAPs) directly have been discovered. They play crucial roles in mitochondrial apoptosis pathways and promote chemotherapy-induced apoptosis. In this study, we constructed a eukaryotic expression vector pcDNA3.1/Smac and transfected it into A549 human lung cancer cells. Then we analyzed the cell invasive and cloning ability, as well as cell apoptosis induced by Taxol. The results showed that over-expressed Smac significantly inhibited A549 cell invasive and cloning ability and promoted apoptosis following Taxol treatment. This finding provides a potential approach for the biological therapy of lung cancer.
Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
