环境类雌激素双酚A通过上调Snail蛋白表达促进MCF-7乳腺癌细胞迁移  

Endocrine disrupting chemicals bisphenol A promoting MCF-7 breast cancer cell migration through upregulating Snail protein expression

作　　者：冷彦[1] 吴艺舟[2] 孙玉洁[1,2] 

机构地区：[1]南京医科大学人类功能基因组重点实验室,江苏南京210029 [2]南京医科大学细胞生物学系,江苏南京210029

出　　处：《南京医科大学学报（自然科学版）》2014年第10期1297-1304,共8页Journal of Nanjing Medical University(Natural Sciences)

基　　金：国家自然科学基金资助(81172091)

摘　　要：目的:探讨外源性双酚A(BPA)调控MCF-7乳腺癌细胞迁移的分子机制。方法:通过划痕实验和Transwell实验检测MCF-7乳腺癌细胞迁移能力,并以黏附实验反向辅助验证;通过质粒转染干扰Snail蛋白表达水平,进一步研究外源性BPA调控MCF-7乳腺癌细胞迁移的分子机制。结果:外源性BPA能上调细胞中Snail的表达水平,从而下调E-cadherin的表达并促进MCF-7乳腺癌细胞迁移;siRNA干扰Snail表达后MCF-7乳腺癌细胞迁移减慢。此外,BPA刺激能降低MCF-7乳腺癌细胞黏附能力。结论:外源性BPA可通过上调Snail表达水平,促进MCF-7乳腺癌细胞的迁移,为进一步阐明乳腺癌细胞侵袭与转移的分子调控机制提供了新线索。Objective：To explore the underlying molecular mechanisms of exogenous bisphenol A（BPA） regulating MCF-7 breast cancer cell migration. Methods： The migration of MCF-7 breast cancer cells was detected by wound healing assay and transwell assay, and further confirmed by adhesion assay. Furthermore, the migratory ratio of MCF-7 breast cancer cells was analyzed by knockdown of Snail. Results： Exogenous BPA was able to increase the expression of Snail in MCF-7 breast cancer cells and decrease the expression of E-cadherin and thus promote cell migration. Knockdown of Snail was able to retard the MCF-7 breast cancer cell migration. Furthermere,BPA stimulation reduced the adhesion ability of MCF-7 breast cancer cells. Conclusion： We demonstrated that exogenous BPA induced MCF-7 breast cancer cell migration by upregulating Snail protein expression. These findings provide a new clue for better understanding the mechanism of breast carcinoma metastasis.

关 键 词：双酚A SNAIL E-CADHERIN MCF-7乳腺癌细胞 迁移 

分 类 号：R737.9[医药卫生—肿瘤]