分子碘在人类乳腺癌细胞细胞凋亡caspase-independent涉及mitochondria-mediated通路。

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Shrivastava,女子M, Sinha RA,库马尔,Balapure AK,亚太区VK, Sharma R, Mitra K,经脉,Godbole毫米

分子碘在人类乳腺癌细胞细胞凋亡caspase-independent涉及mitochondria-mediated通路。

生物化学杂志。2006年7月14日;281 (28):19762 - 71。2006年5月5日Epub。

PubMed ID

16679319 (在PubMed

]

文摘

分子碘(I2)被抑制的感应和推广N-methyl-n-nitrosourea-induced乳腺致癌,回归7,12-dimethylbenz (a) anthracene-induced乳房肿瘤的老鼠,也被证明有有益的作用在人类乳腺纤维囊性的疾病。在人工培养的乳腺癌细胞系细胞毒性的碘,即MCF-7、mda - mb - 231, mda - mb - 453, zr - 75 - 1,和T-47D报道在这个沟通。碘细胞系的诱导细胞凋亡在所有测试,除了mda - mb - 231所示sub-G1高峰使用流式细胞术分析。碘抑制正常的人类外周血单核细胞的增殖;然而,它没有这些细胞中诱导细胞死亡。的iodine-induced MCF-7细胞凋亡机制研究。DNA片段分析证实internucleosomal DNA降解。终端原位dUTP缺口末端标记证实碘以时间和剂量依赖性的方式诱导细胞凋亡在MCF-7细胞。Iodine-induced还存在细胞凋亡是独立的。线粒体膜电位碘消散,表现出抗氧化活性,在总细胞硫醇含量引起的损耗。 Western blot results showed a decrease in Bcl-2 and up-regulation of Bax. Immunofluorescence studies confirmed the activation and mitochondrial membrane localization of Bax. Ectopic Bcl-2 overexpression did not rescue iodine-induced cell death. Iodine treatment induces the translocation of apoptosis-inducing factor from mitochondria to the nucleus, and treatment of N-acetyl-L-cysteine prior to iodine exposure restored basal thiol content, ROS levels, and completely inhibited nuclear translocation of apoptosis-inducing factor and subsequently cell death, indicating that thiol depletion may play an important role in iodine-induced cell death. These results demonstrate that iodine treatment activates a caspase-independent and mitochondria-mediated apoptotic pathway.

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