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Bisphenol A impairs estradiol-induced protective effects against DLD-1 colon cancer cell growth
Article first published online: 10 SEP 2010
DOI: 10.1002/iub.370
Copyright © 2010 International Union of Biochemistry and Molecular Biology, Inc.
Additional Information
How to Cite
Bolli, A., Bulzomi, P., Galluzzo, P., Acconcia, F. and Marino, M. (2010), Bisphenol A impairs estradiol-induced protective effects against DLD-1 colon cancer cell growth. IUBMB Life, 62: 684–687. doi: 10.1002/iub.370
Publication History
- Issue published online: 29 SEP 2010
- Article first published online: 10 SEP 2010
- Manuscript Accepted: 21 JUL 2010
- Manuscript Received: 13 JUL 2010
Funded by
- National Institute of Biostructures and Biosystems (INBB) of Italy
- Italian Health Ministry (Strategico, 2008)
Keywords:
- apoptosis;
- bisphenol A;
- endocrine disruptor;
- 17β-estradiol;
- estrogen receptor β;
- colon cancer cell line
Abstract
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