2-甲基-3-羟基蒽醌诱导人乳腺癌MCF-7细胞凋亡的机制

李娜; 崔瑞杰; 赵小顺; 梁金英

2-甲基-3-羟基蒽醌诱导人乳腺癌MCF-7细胞凋亡的机制

1.
新乡市中心医院药剂科
2.
新乡医学院药学院

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- 刊出日期: 2011-08-24

2-Methyl-3-hydroxy-anthraquinone induces Ca^{2+-mediated apoptosis in human MCF-7 breast cancer cells}

摘要

摘要: 为探讨2-甲基-3-羟基蒽醌抗肿瘤作用及其机制，本研究采用锥虫蓝法检测细胞活力,流式细胞仪检测细胞周期变化、细胞凋亡率、线粒体膜电位及细胞内游离钙的变化，Western blot方法检测凋亡相关蛋白caspase-4、caspase-7、caspase-9、Bcl-2、Bax、JNK、细胞色素C的表达。结果发现：2-甲基-3-羟基蒽醌时间依赖性地抑制乳腺癌细胞的生长，升高细胞内游离钙含量，降低线粒体膜电位并诱导其凋亡；药物上调Bax并下调Bcl-2蛋白的表达；诱导caspase-4、caspase-7、caspase-9、calpain的活化及细胞色素C的释放。结果提示2-甲基-3-羟基蒽醌可能通过Ca²⁺/calpain/caspase-4途径诱导人乳腺癌MCF-7细胞凋亡。
- 2-甲基-3-羟基蒽醌 /
- 凋亡 /
- caspase /
- 钙蛋白酶 /
- 细胞内游离钙
Abstract: To evaluate the mechanism of 2-methyl-3-hydroxy-anthraquinone (MHA) inducing apoptosis in human MCF-7 breast cancer cells.Cell viability was assessed by trypan blue dye exclusion assay,cell cycle distribution,apoptosis and mitochondrial membrane potential and [Ca²⁺]_i were measured by FACScan;the protein expression of caspase-4,caspase-7,caspase-9,Bcl-2,Bax,calpain and cytochrome C in the MCF-7 cells was evaluated by Western blots.The results demonstrated that MHA was able to inhibit cell proliferation in a time-dependent manner.It induced[Ca²⁺]_i overload, decreased mitochondrial membrane potential and finally induced cancer cell apoptosis.Caspase-4, caspase-7, caspase-9 and calpain protein were activated.Bax expression was upregulated and Bcl-2 expression was downregulated.MHA induced MCF-7 cells apoptosis via Ca²⁺ /calpain/caspase-4 pathway.
- 2-methyl-3-hydroxy-anthraquinone /
- apoptosis /
- caspase /
- calpain /
- [Ca²⁺]_i

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2-甲基-3-羟基蒽醌诱导人乳腺癌MCF-7细胞凋亡的机制

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2-Methyl-3-hydroxy-anthraquinone induces Ca2+-mediated apoptosis in human MCF-7 breast cancer cells

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2-Methyl-3-hydroxy-anthraquinone induces Ca^{2+-mediated apoptosis in human MCF-7 breast cancer cells}