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Snail and Slug mediate tamoxifen resistance in breast cancer cells through activation of EGFR–ERK independent of epithelial–mesenchymal transition Free
Yan Jiang1,†, Xiaotong Zhao1,†, Qian Xiao1, Qingbo Liu1, Keshuo Ding2, Fei Yu1, Rui Zhang1, Tao Zhu2, and Gaoxiang Ge1,3,*
1State Key Laboratory of Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China
2Hefei National Laboratory for Physical Sciences, Hefei, Anhui 230027, China
3Cancer Research Center, Shanghai Xu-Hui Central Hospital, Shanghai Clinical Center, Chinese Academy of Sciences, Shanghai 200031, China *Correspondence to:Gaoxiang Ge, E-mail: gxge@sibcb.ac.cn
J Mol Cell Biol, Volume 6, Issue 4, August 2014, 352-354,  https://doi.org/10.1093/jmcb/mju019

Breast cancer is the second most common type of cancer and the leading cause of cancer death in women worldwide. Adjuvant tamoxifen therapy significantly slows down estrogen receptor (ER)-positive breast cancer progression, prolongs disease-free survival, and contributes to the decrease in breast cancer mortality (Musgrove and Sutherland, 2009). However, majority of the death from breast cancer is due to metastasis that is resistant to therapy (Musgrove and Sutherland, 2009). The frequent distant metastasis after therapy implicates that resistance to anti-cancer drugs might be the intrinsic characteristic of metastatic cancer cells. Tamoxifen-resistant breast cancer cells frequently exhibit mesenchymal-like morphology (Hiscox et al., 2006; Kim et al., 2009; Ward et al., 2012; Zhou et al., 2012), enhanced motility (McBryan et al., 2012; Zhou et al., 2012), and epithelial–mesenchymal transition (EMT) gene expression pattern (Iseri et al., 2011). Re-expression of microRNA-375 reverses both tamoxifen resistance and accompanying EMT-like properties in breast cancer (Ward et al., 2012). This promotes us to investigate whether EMT contributes to the acquisition of breast cancer tamoxifen resistance.