2012Unpublished venueRequires access

Hypoxia can induce EMT and promote invasion of breast cancer cells

Fuqiang Jiang, Juyi Wen, Jingbo Kang, Nie Qing

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Abstract

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 Vimeutin 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. Key words: Breast neoplasms;  Anoxia;  Epithelium;  Stromalcells;  Neoplasm invasiveness;  Cel migration

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What this paper is about

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 Vimeutin 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. Key words: Breast neoplasms;  Anoxia;  Epithelium;  Stromalcells;  Neoplasm invasiveness;  Cel migration

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Available abstract

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 Vimeutin 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. Key words: Breast neoplasms;  Anoxia;  Epithelium;  Stromalcells;  Neoplasm invasiveness;  Cel migration

Key concepts: Vimentin, Hypoxia (environmental), Downregulation and upregulation, Metastasis, Cadherin, Western blot, Cancer research, Epithelial–mesenchymal transition

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