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Bisphenol A impairs estradiol‐induced protective effects against DLD‐1 colon cancer cell growth
Author(s) -
Bolli Alessandro,
Bulzomi Pamela,
Galluzzo Paola,
Acconcia Filippo,
Marino Maria
Publication year - 2010
Publication title -
iubmb life
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.132
H-Index - 113
eISSN - 1521-6551
pISSN - 1521-6543
DOI - 10.1002/iub.370
Subject(s) - estrogen receptor , bisphenol a , estrogen , cancer research , cell growth , population , chemistry , medicine , endocrinology , endocrine system , estrogen receptor beta , colorectal cancer , receptor , estrogen receptor alpha , cancer , breast cancer , biology , hormone , biochemistry , environmental health , organic chemistry , epoxy
Bisphenol A (BPA), a prototype of endocrine disruptors, mimics 17β‐estradiol (E2)‐induced proliferation in several cancer cells by binding to estrogen receptor α (ERα). However, scarce and conflicting data are available concerning the effect of BPA on estrogen receptor β (ERβ)‐mediated functions. Here, the detailed analysis of the effect of BPA, alone or in combination with E2, on ERβ‐mediated cellular functions is reported in ERβ‐expressing colon cancer cell line. BPA binds to ERβ without activating any receptor activities. On the other hand, BPA inhibits E2‐induced genomic activity of ERβ as well as ERβ extra‐nuclear activities ( i.e. , ERβ:p38 association and p38 activation). As a consequence, BPA impairs the E2‐induced activation of the apoptotic cascade which is at the root of the protective role played by the hormone against colon cancer growth. Thus, women may be considered a highly susceptible population with an increased risk of colon cancers after BPA exposures. © 2010 IUBMB IUBMB Life, 62(9): 684–687, 2010