Journal
MOLECULAR AND CELLULAR ENDOCRINOLOGY
Volume 418, Issue -, Pages 193-206Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.mce.2015.04.017
Keywords
ER-alpha 36; Rapid estrogen signaling; ER-positive and -negative breast cancer; Breast cancer stem/progenitor cells; Antiestrogen resistance
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Funding
- Department of Defense [DAMD 11-1-0497]
- Nebraska Tobacco Settlement Biomedical Research Program [LB-595]
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Prevailing wisdom is that estrogen receptor (ER)-alpha mediated genomic estrogen signaling is responsible for estrogen-stimulated cell proliferation and development of ER-positive breast cancer. However, accumulating evidence indicates that another estrogen signaling pathway, non-genomic or rapid estrogen signaling, also plays an important role in mitogenic estrogen signaling. Previously, our laboratory cloned a 36 kDa variant of ER-alpha, ER-alpha 36, and found that ER-alpha 36 is mainly expressed in the cytoplasm and at the plasma membrane. ER-alpha 36 mediates rapid estrogen signaling and inhibits genomic estrogen signaling. In this review, we review and update the biological function of ER-alpha 36 in ER-positive and -negative breast cancer, breast cancer stem/progenitor cells and tamoxifen resistance, potential interaction and cross-talk of ER-alpha 36 with other ERs and growth factor receptors, and intracellular pathways of ER-alpha 36-mediated rapid estrogen signaling. The potential function and underlying mechanism of ER-alpha in development of ER-positive breast cancer will also be discussed. (C) 2015 Elsevier Ireland Ltd. All rights reserved.
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