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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Efficacy of the dietary histone deacetylase inhibitor butyrate alone or in combination with vitamin A against proliferation of MCF-7 human breast cancer cells

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Author(s):
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Andrade, F. O. [1] ; Nagamine, M. K. [2] ; De Conti, A. [1] ; Chaible, L. M. [2] ; Fontelles, C. C. [1] ; Jordao Junior, A. A. [3] ; Vannucchi, H. [3] ; Dagli, M. L. Z. [2] ; Bassoli, B. K. [1] ; Moreno, F. S. [1] ; Ong, T. P. [1]
Total Authors: 11
Affiliation:
[1] Univ Sao Paulo, Fac Ciencias Farmaceut, Dept Alimentos & Nutr Expt, Lab Dieta Nutr & Canc, BR-05508900 Sao Paulo - Brazil
[2] Univ Sao Paulo, Fac Med Vet & Zootecnia, Dept Patol, Expt Oncol Lab, BR-05508900 Sao Paulo - Brazil
[3] Univ Sao Paulo, Fac Med Ribeirao Preto, Dept Clin Med, Div Nutr, Ribeirao Preto, SP - Brazil
Total Affiliations: 3
Document type: Journal article
Source: Brazilian Journal of Medical and Biological Research; v. 45, n. 9, p. 841-850, SEP 2012.
Web of Science Citations: 4
Abstract

The combined treatment with histone deacetylase inhibitors (HDACi) and retinoids has been suggested as a potential epigenetic strategy for the control of cancer. In the present study, we investigated the effects of treatment with butyrate, a dietary HDACi, combined with vitamin A on MCF-7 human breast cancer cells. Cell proliferation was evaluated by the crystal violet staining method. MCF-7 cells were plated at 5 x 10(4) cells/mL and treated with butyrate (1 mM) alone or combined with vitamin A (10 mu M) for 24 to 120 h. Cell proliferation inhibition was 34, 10 and 46% following treatment with butyrate, vitamin A and their combination, respectively, suggesting that vitamin A potentiated the inhibitory activities of butyrate. Furthermore, exposure to this short-chain fatty acid increased the level of histone H3K9 acetylation by 9.5-fold (Western blot), but not of H4K16, and increased the expression levels of p21(WAF1) by 2.7-fold (Western blot) and of RAR beta by 2.0-fold (quantitative real-time PCR). Our data show that RAR beta may represent a molecular target for butyrate in breast cancer cells. Due to its effectiveness as a dietary HDACi, butyrate should be considered for use in combinatorial strategies with more active retinoids, especially in breast cancers in which RAR beta is epigenetically altered. (AU)