论文部分内容阅读
The biological activity of adriamycin was investigated in human breast carcinoma (HBC) cells. Adri-amycin inhibited the growth of a number of HBC cell lines and induced G1 arrest followed by apoptosis. In MCF-7 cells that harbor wild-type p53, adriamycin-induced G1 arrest and apoptosis was accompanied by p53-independent regulation of WAF1/CIP1 as well as bax mRNA levels. In MDA-MB-231 cells which possess a mutant p53, adriamycin-induced G1 arrest and apoptosis was also associated with a cpncomitant up-regulation of WAF1/CIP1 mRNA while these cells did not express bax or bcl-2 messages. Thus, adriamycin induces G1 arrest and apoptosis via a unique pathway which appears to involve activation of downstream effectors of p53-independent manner.
The biological activity of adriamycin was investigated in human breast carcinoma (HBC) cells. Adri-amycin inhibited the growth of a number of HBC cell lines and induced G1 arrest followed by apoptosis. In MCF-7 cells that harbor wild-type p53, adriamycin -induced G1 arrest and apoptosis was accompanied by p53-independent regulation of WAF1 / CIP1 as well as bax mRNA levels. In MDA-MB-231 cells which possess a mutant p53, adriamycin-induced G1 arrest and apoptosis was also associated with a cpncomitant up-regulation of WAF1 / CIP1 mRNA while these cells did not express bax or bcl-2 messages. Thus, adriamycin induces G1 arrest and apoptosis via a unique pathway which appears to involve activation of downstream effectors of p53-independent manner.