Associated effects of sodium butyrate on histone acetylation and estrogen receptor in the human breast cancer cell line MCF-7

Stevens, M.Sandra; Aliabadi, Zarrintaj; Moore, Michael R.

doi:10.1016/0006-291x(84)91628-0

Cited by 27 publications

(12 citation statements)

References 30 publications

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“…Indeed, in cells expressing high levels of ERa such as MCF-7 cells, ERa mRNA and protein are strongly reduced as previously shown by other studies (Stevens et al, 1984). However, the effects of HDI on ERa levels are complex since in ERa-negative cells, we observed that TSA treatment reactivated ERa expression (data not shown), which is in agreement with previous studies (Yang et al, 2000).…”

Section: Discussionsupporting

confidence: 93%

ERα and ERβ expression and transcriptional activity are differentially regulated by HDAC inhibitors

et al. 2005

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The proliferative action of ERa largely accounts for the carcinogenic activity of estrogens. By contrast, recent data show that ERb displays tumor-suppressor properties, thus supporting the interest to identify compounds that could increase its activity. Here, we show that histone deacetylase inhibitors (HDI) upregulated ERb protein levels, whereas it decreased ERa expression. Part of this regulation took place at the mRNA level through a mechanism independent of de novo protein synthesis. In addition, we found that, in various cancer cells, the treatment with different HDI enhanced the liganddependent activity of ERb more strongly than that of ERa. On the other hand, in MDA-MB231 and HeLa cells, the expression of ERs modified the transcriptional response to HDI. The use of deletion mutants of both receptors demonstrated that AF1 domain of the receptors was required. Finally, we show that ERb expression led to a dramatic increased in the antiproliferative activity of HDI, which correlated with a modification of the transcription of genes involved in cell cycle control by HDI. Altogether, these data demonstrate that the interference of ERb and HDAC on the control of transcription and cell proliferation constitute a promising approach for cancer therapy.

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Section: Discussionsupporting

confidence: 93%

ERα and ERβ expression and transcriptional activity are differentially regulated by HDAC inhibitors

et al. 2005

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“…Deacetylases hydrolyse acetyl groups covalently attached to the e-amino group of lysine residues not only from histones but also from nonhistone proteins, whose activity may be regulated by post translational acetylation (Bannister and Miska, 2000). We previously reported that TSA provokes clearance of ERa from the breast carcinoma cell line MCF-7 , extending a previous report that butyric acid may also induce removal of ERa from cells (Stevens et al, 1984). More recently, Alao et al (2004) also demonstrate that TSA represses ERa mRNA synthesis.…”

Section: Introductionmentioning

confidence: 53%

Multiple mechanisms induce transcriptional silencing of a subset of genes, including oestrogen receptor α, in response to deacetylase inhibition by valproic acid and trichostatin A

et al. 2005

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Valproate (VPA) and trichostatin A (TSA), inhibitors of zinc-dependent deacetylase activity, induce reduction in the levels of mRNA encoding oestrogen receptor-a (ERa), resulting in subsequent clearance of ERa protein from breast and ovarian cell lines. Inhibition of oestrogen signalling may account for the endocrine disorders, menstrual abnormalities, osteoporosis and weight gain that occur in a proportion of women treated with VPA for epilepsy or for bipolar mood disorder. Transcriptome profiling revealed that VPA and TSA also modulate the expression of, among others, key regulatory components of the cell cycle. Meta-analysis of genes directly responsive to oestrogen indicates that VPA and TSA have a generally antioestrogenic profile in ERa positive cells. Concomitant treatment with cycloheximide prevented most of these changes in gene expression, including downregulation of ERa mRNA, indicating that a limited number of genes signal a hyperacetylated state within cells. Three members of the NAD-dependent deacetylases, the sirtuins, are upregulated by VPA and by TSA and sirtuin activity contributes to loss of ERa expression. However, prolonged inhibition of the sirtuins by sirtinol also induces loss of ERa from cells. Mechanistically, we show that VPA invokes reversible promoter shutoff of the ERa, pS2 and cyclin D1 promoters, by inducing recruitment of methyl cytosine binding protein 2 (MeCP2) with concomitant exclusion of the maintenance methylase DNMT1. Furthermore, we demonstrate that, in the presence of VPA, local DNA methylation, deacetylation and demethylation of activated histones and recruitment of inhibitory complexes occurs on the pS2 promoter.

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“…In addition butyrate has a variety of effects on cellular function, which cannot be satisfactory explained by its action as a histone deacetylase inhibitor (3)(4)(5)(6)(7).…”

Section: Introductionmentioning

confidence: 99%

RNA polymerase activity and template activity of chromatin after butyrate induced hyperacetylation of histones inPhysarum

Loidl¹,

Loidl²,

Puschendorf³

et al. 1984

Nucl Acids Res

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Associated effects of sodium butyrate on histone acetylation and estrogen receptor in the human breast cancer cell line MCF-7

Cited by 27 publications

References 30 publications

ERα and ERβ expression and transcriptional activity are differentially regulated by HDAC inhibitors

ERα and ERβ expression and transcriptional activity are differentially regulated by HDAC inhibitors

Multiple mechanisms induce transcriptional silencing of a subset of genes, including oestrogen receptor α, in response to deacetylase inhibition by valproic acid and trichostatin A

RNA polymerase activity and template activity of chromatin after butyrate induced hyperacetylation of histones inPhysarum

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