Data show that the mechanism by which fibroblast growth factor 2 protects small cell lung cancer cells from etoposide-induced cell death involves inhibition of Smac release but not of cytochrome c release.

Smac deficiency may be compensated for by action of redundant determinants to kill cancer cells. Thus, translocation of endogenous Smac into cytosol does not play a critical role in cell death of human lung carcinoma after etoposide treatment.

Thus, survivin, Smac, and PKC alpha might play important roles in the inhibition of apoptosis by FGF-2 in human small cell lung cancer cells.

Our data suggest that assessment of survivin and second mitochondria-derived activator of caspase mRNA expression may be useful for predicting survival in non-small cell lung cancer patients receiving platinum-based chemotherapy after surgical resection

Results indicate important roles of Smac in suppressing lung cancer cell growth and sensitivity to chemotherapeutic drugs.

Overexpression of Smac promotes Cisplatin-induced apoptosis by activating caspase-3 and caspase-9 in lung cancer.

Study found a negative correlation between Smac and XIAP at the level of protein but not mRNA in non-small cell lung carcinoma (NSCLC) patients. Overexpressed XIAP could degrade through ubiquitination, the mature Smac inhibiting NSCLC apoptosis.

Targeting bone morphogenetic protein receptor 2 sensitizes lung cancer cells to TRAIL by increasing cytosolic Smac/DIABLO and the downregulation of X-linked inhibitor of apoptosis protein.