Abstract:
:Estrogen nuclear receptors, represented by the canonical forms ERα66 and ERβ1, are the main mediators of the estrogen-dependent pathophysiology in mammals. However, numerous isoforms have been identified, stimulating unconventional estrogen response pathways leading to complex cellular and tissue responses. The estrogen receptor variant, ERα36, was cloned in 2005 and is mainly described in the literature to be involved in the progression of mammary tumors and in the acquired resistance to anti-estrogen drugs, such as tamoxifen. In this review, we will first specify the place that ERα36 currently occupies within the diversity of nuclear and membrane estrogen receptors. We will then report recent data on the impact of ERα36 expression and/or activity in normal breast and testicular cells, but also in different types of tumors including mammary tumors, highlighting why ERα36 can now be considered as a marker of malignancy. Finally, we will explain how studying the regulation of ERα36 expression could provide new clues to counteract resistance to cancer treatments in hormone-sensitive tumors.
journal_name
Int J Mol Scijournal_title
International journal of molecular sciencesauthors
Thiebaut C,Konan HP,Guerquin MJ,Chesnel A,Livera G,Le Romancer M,Dumond Hdoi
10.3390/ijms21114116subject
Has Abstractpub_date
2020-06-09 00:00:00issue
11issn
1422-0067pii
ijms21114116journal_volume
21pub_type
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