Journal
MOLECULAR AND CELLULAR ENDOCRINOLOGY
Volume 314, Issue 1, Pages 17-22Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.mce.2009.09.011
Keywords
Breast cancer; ER alpha; HD1; VPA; Antiestrogen
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Funding
- MIUR
- Regione Piemonte
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Histone deacetylase inhibitors (HDIs) are valuable drugs in breast cancer where estrogen receptor a (ER alpha) can be silenced by epigenetic modifications. We report the effect of the clinically available HDI, valproic acid (VPA), on ER alpha expression and function in ER-negative breast cancer cells, MDA-MB-231. VPA induced ER(x mRNA and protein, while did not modify ER beta. In VPA-treated cells, we also observed: (1) a correct transcriptional response to estradiol after transfection with the luciferase gene under the control of an estrogen-responsive minimal promoter (ERE-TKluc); (2) increased expression of the ER-related transcription factor FoxA1; (3) estradiol-induced up-regulation of several estrogen-regulated genes (e.g. pS2, progesterone receptor); (4) inhibitory effect of tamoxifen on cell growth. In conclusion, the HDI VPA, inducing ER alpha and FoxA1, confers to MDA-MB 231 cells an estrogen-sensitive phenotype, restoring their sensitivity to antiestrogen therapy. (C) 2009 Elsevier Ireland Ltd. All rights reserved.
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