[[abstract]]VP-16 (etoposide), an inhibitor of topoisomerase IIα, was widely used for cancer therapy. We found low dosage of VP-16 causes apoptosis in cancer cells without functional p53. In this work, we have identified that caspases were responsible for the progression of apoptosis in VP-16-induced H1299 cells lacking endogenous p53. Further study showed that apoptosis effectors caspase-9 and caspase-7 were activated prior to apoptosis. This work also demonstrated that VP-16-induced apoptosis in human non-small cell lung cancer cells is independent of p53 status.
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