Driving p53 response to Bax activation greatly enhances sensitivity to taxol by inducing massive apoptosis.

摘要: The proapoptotic gene bax is one of the downstream effectors p53. p53 binding site in promoter less responsive to than growth arrest mediating p21. We introduced under control 13 copies a strong element into two ovarian cancer cell lines. clones expressing obtained from wild-type (wt) p53-expressing line A2780 were much more sensitive (500- 1000-fold) anticancer agent taxol parent line, with higher percentage cells undergoing apoptosis after drug treatment that was clearly p53-dependent and bax-mediated. Xenografts established nude mice selected clone (A2780/C3) parental apoptotic response A2780/C3 tumors also increased treatment. Introduction same plasmid null SKOV3 did not alter sensitivity or induction apoptosis. In conclusion, driving (after treatment) by activating rather p21 results massive apoptosis, vitro vivo, greatly enhances drug.