吉西他滨对乳腺癌MCF-7细胞凋亡及其caspase-8活性的影响

Study on caspase-8 in apoptoss of breast cancer cell line MCF-7 cells induced by gemcibine

目的探讨吉西他滨诱导乳腺癌M CF-7细胞凋亡及其与天冬氨酸特异的半胱氨酸蛋白酶(cas-pase)-8活性变化的关系。方法观察吉西他滨诱导M CF-7细胞的凋亡及加入caspase-8抑制剂异亮氨酰—谷氨酰—苏氨酰—天冬氨酰—氟甲基酮(IETD-FM K)后M CF-7细胞凋亡率及其caspase-8活性的变化。结果吉西他滨作用2 d后,凋亡细胞比例随吉西他滨浓度的增加而升高;加入IE ID-FM K则凋亡率显著下降。不同浓度的吉西他滨均可诱导M CF-7细胞caspase-8活性增高,高浓度与低浓度比较差异有显著性(P<0.01)。IE ID-FM K能阻断caspase-8活化而抑制M CF-7细胞凋亡。结论吉西他滨可通过caspase-8信号转导途径诱导乳腺癌细胞发生凋亡,并呈时间和浓度依赖性。

Objective ： To investigate the role of caspase-8 in apoptosis of MCF-7 cells induced by gemcitabine. Methods： Flow cytometry was used to analyze the apoptotic rates of MCF-7 cells induced by gemcitabine with or without the caspase-8 inhibitor IEID-FMK. The caspase-8 activity was detected by using caspase-8 Fluorescent Assay Kit. Results：Two days after MCF-7 cells were treated with gemcitabine at different concentration, the apoptotic rates and caspase-8 activity increased gradually with gemcitabine concentration scalar increasing. IEID-FMK could block the activation of Caspase-8 and reduced the apoptosis of MCF-7 induced by Gemcitabine. Conclusions： The apoptosis of MCF-7 cells could be induced by gemcitabine via caspase-8-transducted signal pathway in a time and concentration-dependent manner.