Role of ER-α36 in breast cancer by typical xenoestrogens

Tumour Biol. 2015 Sep;36(10):7355-64. doi: 10.1007/s13277-015-4006-x. Epub 2015 Sep 4.

Abstract

About 10 years have passed since the discovery of the estrogen receptor subtype, estrogen receptor alpha 36 (ER-α36). The relationship between cancerous cells and ER-α36 in mediating xenoestrogens (XEs) is a significant issue in the progression and treatment of breast cancer. XEs can combine with classical estrogen receptors and other receptor subtypes especially ER-α36, resulting in activation of nongenomic pathways as well as genomic pathways. Recently, most laboratories have focused on further study into the rapidly nongenomic mechanisms by overexpressing or knocking down ER-α36 in breast cancer cell lines. These rapid responses can induce the deregulation of cell cycle, and then lead to the abnormal proliferation and differentiation by regulating distinct downstream pathways. It appears that ER-α36 is a key factor in increasing risk of breast cancer. However, in several recent studies, the action mechanisms of ER-α36 by XEs in breast cancer cell lines are not always clear. In this review, we firstly summarize the expression pattern and tumor biology of ER-α36, then discuss these related estrogenic effects of ER-α36, and lastly give the predictive and prognostic value of ER-α36 as diagnostic marker by mediating typical XEs in breast cancer.

Keywords: Breast cancer; ER-α36; Estrogenic effects; Predictive and prognostic value; Xenoestrogens.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Breast Neoplasms / drug therapy*
  • Breast Neoplasms / metabolism*
  • Estrogen Receptor alpha / metabolism*
  • Estrogens / pharmacology*
  • Female
  • Humans

Substances

  • Estrogen Receptor alpha
  • Estrogens