柳氮磺口比口定水楊酸與鐵誘發乳癌細胞MDA-MB-231鐵依賴性死亡初探

林亞葳

doi:10.6342/NTU201603493

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柳氮磺口比口定水杨酸与铁诱发乳癌细胞MDA-MB-231铁依赖性死亡初探

Ferroptosis Induction in Breast Cancer Cell Line MDA-MB-231 by Sulfasalazine and Ferric Ammonium Citrate

林亚葳 , 硕士　　导师：萧宁馨　　

繁体中文 DOI： 10.6342/NTU201603493

铁依赖性死亡；铁；乳癌；水杨酸； Ferroptosis ； Iron ； Breast Cancer ； Sulfasalazine

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摘要 │ 参考文献 (142) │ 国际计量

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Iron plays dual roles in cells. It is essential for cell growth but also produce reactive oxygen species (ROS) via the Fenton reaction then inducing cell toxicity and damage. Iron-dependent cell death, ferroptosis, is a newly discovered non-apoptotic cell death mode in 2003. It is a regulated form of cell death driven by iron-induced lipid peroxide accumulation and regulation strictly by intracellular signaling pathway. The morphological, biochemical markers and genetic characteristics of ferroptosis are different from apoptosis, necrosis and autophagic. The mechanism of ferroptosis is inhibiting synthesis and utilization of reduced-glutathione (GSH) . Then, GSH depletion and lipid peroxide (LROS) accumulation lead to ferroptosis. Blockade of any steps is might prevent ferroptosis. Breast cancer cells have the ability of iron accumulation, which increases breast cancer cells growth. The higher malignancy degrees of breast cancer cells have the stronger ability of iron accumulation. Therefore, the purpose of this study is investigating the effect of ferroptosis on breast cancer cell. The study design is making use of the two characteristics of triple-negative breast cancer cell line MDA-MB-231 : sensitive to sulfasalazine (SAS) and strong ability of iron accumulation, to induce ferroptosis. We detect ferroptosis molecular characteristics, and the effects is blocked by specific inhibitors ferrostatin-1. Then, we analyze iron-related antioxidant proteins NRF2, HO-1 and ferritin (FTH) protein expression and assess the impact of the antioxidant mineral selenium and zinc compound in ferroptosis. The results show that combined group (SAS + iron) induce MDA-MB-231 cells ferroptosis, and ferrostatin-1 inhibit cell death. In addition, ROS and LROS are increased before cell death. The NRF2 and FTH protein expression levels are increased in a combined group dose-dependent manner. Finally, we found selenium can inhibit ferroptosis, and the mechanism may be through increasing the GPX4 protein expression. Zinc increase cell death in combined group and enhance Zn-MT protein expression, but Zn-MT does not contribute to prevent cell death.

参考文献 ( 142 ) 〈TOP〉

1.　Hentze MW, Muckenthaler MU, Galy B, Camaschella C. Two to tango: regulation of mammalian iron metabolism. Cell 2010; 142: 24-38.
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2.　Arora S. Iron Metabolism. InTech, 2012.
连结：
4.　Bogdan AR, Miyazawa M, Hashimoto K, Tsuji Y. Regulators of iron homeostasis: New players in metabolism, cell death, and disease. Trends Biochem Sciences 2016; 41: 274-286.
连结：
5.　Haile D, Hentze M, Rouault T, Harford J, Klausner R. Regulation of interaction of the iron-responsive element binding protein with iron-responsive RNA elements. Molecular and Cellular Biology 1989; 9: 5055-5061.
连结：
6.　Rouault TA, Tang CK, Kaptain S, Burgess WH, Haile DJ, Samaniego F et al. Cloning of the cDNA encoding an RNA regulatory protein--the human iron-responsive element-binding protein. Proceedings of the National Academy of Sciences 1990; 87: 7958-7962.
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使用DOI作为永久连结

引用含有DOI的文献

DOI可强化引用精确性、增强学术圈连结，并给予使用者跨平台的良好使用经验，目前在全世界已有超过五千万个对象申请DOI。 如想对DOI的使用与概念有进一步了解，请参考 （ ） 。

DOI可强化引用精确性、增强学术圈连结，并给予使用者跨平台的良好使用经验，目前在全世界已有超过五千万个对象申请DOI。如想对DOI的使用与概念有进一步了解，请参考（）。