Oncotarget

Research Papers:

ERα inhibits epithelial-mesenchymal transition by suppressing Bmi1 in breast cancer

Xiao-Long Wei _, Xiao-Wei Dou, Jing-Wen Bai, Xiang-Rong Luo, Si-Qi Qiu, Di-Di Xi, Wen-He Huang, Cai-Wen Du, Kwan Man and Guo-Jun Zhang

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Oncotarget. 2015; 6:21704-21717. https://doi.org/10.18632/oncotarget.3966

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Abstract

Xiao-Long Wei1,2, Xiao-Wei Dou2, Jing-Wen Bai2, Xiang-Rong Luo2, Si-Qi Qiu3, Di-Di Xi2, Wen-He Huang3, Cai-Wen Du4, Kwan Man5, Guo-Jun Zhang2,3

1Department of Pathology, Cancer Hospital of Shantou University Medical College, Shantou 515031, China

2Changjiang Scholar’s Laboratory and Cancer Research Center, Shantou University Medical College, Shantou 515031, China

3The Breast Center, Cancer Hospital of Shantou University Medical College, Shantou 515031, China

4Department of Breast Medical Oncology, Cancer Hospital of Shantou University Medical College, Shantou 515031, China

5Department of Surgery and Transplantation, Li Ka Shing Faculty of Medicine, Hong Kong University, Hong Kong 999077, China

Correspondence to:

Guo-Jun Zhang, e-mail: guoj_zhang@yahoo.com

Keywords: ERα signaling, epithelial-mesenchymal transition, Bmi1, breast cancer, stemness

Received: October 20, 2014     Accepted: April 30, 2015     Published: May 13, 2015

ABSTRACT

In human breast cancer, estrogen receptor-α (ERα) suppresses epithelial–mesenchymal transition (EMT) and stemness, two crucial parameters for tumor metastasis; however, the underlying mechanism by which ERα regulates these two processes remains largely unknown. Bmi1, the polycomb group protein B lymphoma Mo-MLV insertion region 1 homolog, regulates EMT transition, maintains the self-renewal capacity of stem cells, and is frequently overexpressed in human cancers. In the present study, ERα upregulated the expression of the epithelial marker, E-cadherin, in breast cancer cells through the transcriptional down-regulation of Bmi1. Furthermore, ERα overexpression suppressed the migration, invasion, and EMT of breast cancer cells. Notably, overexpression of ERα significantly decreased the CD44high/CD24low cell population and inhibited the capacity for mammosphere formation in ERα-negative breast cancer cells. In addition, overexpression of Bmi1 attenuated the ERα-mediated suppression of EMT and cell stemness. Immunohistochemistry revealed an inverse association of ERα and Bmi1 expression in human breast cancer tissue. Taken together, our findings suggest that ERα inhibits EMT and stemness through the downregulation of Bmi1.


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