缺氧能引起EMT的发生促进乳腺癌的侵袭和迁移

 目的　探讨缺氧对人类乳腺癌细胞MCF-7上皮-间质转化（ EMT）标志分子E-钙黏着素（E-cadherin）、波型蛋白（Vimentin）及侵袭迁移能力的影响，揭示缺氧引起乳腺癌侵袭转移的机制， 为临床治疗乳腺癌提供实验及理论依据。方法　采用Western blot检测低氧诱导因子-1α（HIF-1α）、E-cadherin、Vimentin的变化；四甲基偶氮唑蓝（MTT）法检测缺氧对人类乳腺癌细胞MCF-7黏附能力的影响；Transwell侵袭小室法检测缺氧对MCF-7细胞侵袭和迁移能力的影响。结果　随着缺氧时间的延长，人类乳腺癌细胞中E-cadherin表达明显降低（0.09±0.02）（t＝30.98，P＝0.0007），Vimentin表达明显升高（0.69±0.04）（t＝915，P＝0.0000) ；缺氧72 h组MCF-7细胞黏附（81.23±0.74）（t＝82.05，P＝0.000）、侵袭（120±6） （t＝22.78，P＝0.0009）和迁移能力明显增强（190±6）（t＝23.49，P＝0.000）。结论　缺氧能下调E-cadherin、上调Vimentin而引起EMT的发生，促进MCF-7细胞黏附、侵袭和迁移。

Hypoxia can induce EMT and promote invasion of breast cancer cells

Objective To study the effect of hypoxia on EMT molecule E-cadherin, Vimentin and invasion of human breast cancer MCF-7 cells, reveal the mechanism of breast cancer invasion and metastasis and provide experimental and theoretical basis. Methods Western blot was used to observe the change of HIF-1α, E-cadherin and Vimentin during hypoxia on MCF-7. MTT was used to study the effects of viability. Transwell chamber was used to detect the ability of invasion and metastasis. Results The expression of E-cadherin was significantly lower （0.09±0.02） （t=30.98 ,P=0.0007） and the expression of Vimentin was significantly higher （0.69±0.04） （t=915,P=0.0000） with the extension of hypoxia. The capability of adhesion （81.23±0.74） （t=82.05,P=0.000）, invasion（120±6） （t=-22.78,P=0.0009） and migration（190±6） （t=23.49,P=-0.000） was significantly increased after 72 h hypoxia（P〈0.05）. Conclusion Hypoxia can downregulate E-cadherin and upregulate Vimentin and enhance the adhesion, invasion and migration of MCF-7.