bcl-2 Protein Inhibits Etoposide-induced Apoptosis through Its Effects on Events Subsequent to Topoisomerase II-induced DNA Strand Breaks and Their Repair

摘要: Abstract Previous studies have shown that bcl-2 overexpression can inhibit apoptosis induced by DNA-damaging agents widely used in cancer chemotherapy, including X-irradiation, alkylating (hydroperoxycyclophosphamide, etc.), and topoisomerase II inhibitors (etoposide, etc.). However, little is known about the mechanism which inhibits triggered these agents. In this study, we examined whether could effects on etoposide-induced DNA damage its repair. For experiments, developed CH31 clones (mouse B-cells) stably transfected with human sense plasmids compared a parental clone or antisense plasmids. Overexpression of protein inhibited cytotoxicity. there was no difference production repair DNa-protein cross-links, single-strand breaks, double-strand breaks among These findings indicate ( ) cytotoxicity etoposide be separated into early events (formation breaks) later (secondary fragmentation cell death) b at some steps between events.