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机构地区:[1]第二军医大学附属长海医院病理科,上海200433
出 处:《临床与实验病理学杂志》2001年第1期45-48,共4页Chinese Journal of Clinical and Experimental Pathology
摘 要:目的 :了解bcl 2 /bax在乳腺癌细胞的p5 3依赖性凋亡和 p5 3非依赖性凋亡中的作用。 方法 :用原位杂交的方法检测化疗药物VM 2 6诱导人乳腺癌细胞株MCF 7和MDA MB 435S凋亡前后bcl 2和bax的mRNA表达情况。结果 :与MDA MB 435S细胞相比 ,MCF 7细胞的bcl 2mRNA水平较高。两株细胞均能在VM 2 6的作用下发生凋亡。药物诱导后 ,MCF 7细胞的bcl 2mRNA表达下降 ,baxmRNA表达增加 ;MDA MB 435S细胞的baxmRNA表达增加 ,bcl 2mRNA无明显变化。结论 :wtp5 3可在转录水平调节bcl 2 /bax的表达 ,从而介导凋亡作用 ;bax在p5 3非依赖性凋亡中也发挥一定作用 ;bcl 2的高表达可能与肿瘤耐药性有关。Purpose To investigate the function of bcl 2/bax in p53 dependent and p53 independent apoptosis of breast cancer cells. Method Using in situ hybridyzation, bcl 2 and bax mRNA levels were detected in human breast cancer cell lines MCF 7 and MDA MB 435S before and after treatment with VM 26. Results bcl 2 mRNA expression was found higher in MCF 7 than in MDA MB 435S. Both the cell lines could be induced apoptosis by VM 26. In VM 26 treated MCF 7, bcl 2 mRNA was down regulated, while bax mRNA expression increased. Bax up regulation and higher AI were also found in VM 26 treated MDA MB 435S. Conclusions wt p53 mediates apoptosis by transcriptional regulating the expression of bcl 2/bax. bax may also have effects on p53 independent apoptosis. High expression of bcl 2 may be related to chemoresistance of tumor.
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