Genes modulated by histone acetylation as new effectors of butyrate activity

Ragione, Fulvio Della; Criniti, Vittoria; Pietra, Valentina Della; Borriello, Adriana; Oliva, Adriana; Indaco, Stefania; Yamamoto, Tadashi; Zappia, Vincenzo

doi:10.1016/s0014-5793(01)02539-x

Cited by 142 publications

(116 citation statements)

References 42 publications

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“…Based on the present results together with those of previous studies [5,6,[9][10][11][12][13][14], we suggest that a decrease in cell cycle-related genes in cluster IV (Table S2) may be closely associated with the cell growth arrest induced by SB. Of particular interest is our identification of the cell cycle-associated genetic network whose core contains CCND1, PCNA and BRCA1 (Fig.…”

Section: Discussionsupporting

confidence: 85%

Genetic networks responsive to sodium butyrate in colonic epithelial cells

et al. 2006

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We performed microarray and computational gene network analyses to identify the detailed mechanisms by which sodium butyrate (SB) induces cell growth arrest and the differentiation of mouse colonic epithelial MCE301 cells. Two thousand six hundred four differentially expressed probe sets were identified in the cells treated with 2 mM SB and were classified into four groups. Of these, the gradually increased group and the gradually and remarkably decreased group contained the genetic networks for cellular development and cell cycles or canonical pathways for fatty acid biosynthesis and pyrimidine metabolism, respectively. The present results provide a basis for understanding the detailed molecular mechanisms of action of SB in colonic epithelial cells.

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Section: Discussionsupporting

confidence: 85%

Genetic networks responsive to sodium butyrate in colonic epithelial cells

et al. 2006

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“…Consistent with this observation is the demonstration of the activation of the HLA-G gene in tumor cell lines treated with the DNA-demethylating drug 5-Aza-dC. Therefore, treatment blocking HDAC and͞or reversing DNA methylation (69,70), and the presence of a specific cytokine microenvironment such as IL-10 (28) or IFNs (26), might favor enhancement of HLA-G transcription and protein expression in tumors and in some inflammatory processes. This finding suggests that the immunogenicity and tumorigenicity of various tumors may be potentially changed according to treatment.…”

Section: Discussionmentioning

confidence: 55%

HLA-G gene repression is reversed by demethylation

Moreau

Mouillot

Rousseau

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

139

134

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The HLA-G molecule plays an important role in immune tolerance, protecting the fetus from maternal immune attack, and probably contributes to graft tolerance and tumor escape from the host immune system. HLA-G expression is tightly regulated and involves mechanisms acting in part at the transcriptional level. Nevertheless, almost all regulatory sequences that govern constitutive and inducible HLA class I gene transcription are disrupted in the HLA-G gene promoter, suggesting an unusual regulatory process. In further investigating the molecular mechanisms of HLA-G gene activation, we evaluated the influence of epigenetic mechanisms on seven HLA-G-negative cell lines that exhibit various phenotypes. Exposure of cells to histone deacetylase inhibitors, or to the demethylating agent 5-aza-2 -deoxycytidine, revealed that HLA-G gene transcription is inhibited by DNA methylation. Reversal of methylation-mediated repression may directly induce HLA-G cellsurface expression, supporting the idea that HLA-G might be activated by such a mechanism during malignancy, inflammation, and allogenic reactions.

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“…The inhibition of HDAC deacetylase activity by TSA results in an increase or a decrease in the expression of a limited number (2-5%) of genes (30,31). Recent reports show the induction of p21 gene by HDACi through the Sp1 element in p21 promoter (26,27).…”

Section: Resultsmentioning

confidence: 99%

Modulation of the Cyclin-Dependent Kinase Inhibitor p21WAF1/Cip1 Gene by Zac1 through the Antagonistic Regulators p53 and Histone Deacetylase 1 in HeLa Cells

Liu

Chan

Lin

et al. 2008

Molecular Cancer Research

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Zac1 is a novel seven -zinc finger protein which possesses the ability to bind specifically to GC-rich DNA elements. Zac1 not only promotes apoptosis and cell cycle arrest but also acts as a transcriptional cofactor for p53 and a number of nuclear receptors. Our previous study indicated that the enhancement of p53 activity by Zac1 is much more pronounced in HeLa cells compared with other cell lines tested. This phenomenon might be due to the coactivator effect of Zac1 on p53 and the ability of Zac1 to reverse E6 inhibition of p53. In the present study, we showed that Zac1 acted synergistically with either p53 or a histone deacetylase inhibitor, trichostatin A, to enhance p21 WAF1/Cip1 promoter activity. We showed that Zac1 physically interacted with some nuclear receptor corepressors such as histone deacetylase 1 (HDAC1) and mSin3a, and the induction of p21 WAF1/Cip1 gene and protein by Zac1 was suppressed by either overexpressing HDAC1 or its deacetylase-dead mutant. In addition, our data suggest that trichostatin A -induced p21 WAF1/Cip1 protein expression might be mediated through a p53-independent and HDAC deacetylaseindependent pathway. Taken together, our data suggest that Zac1 might be involved in regulating the p21 WAF1/Cip1 gene and protein expression through its protein-protein interaction with p53 and HDAC1 in HeLa cells.

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Genes modulated by histone acetylation as new effectors of butyrate activity

Cited by 142 publications

References 42 publications

Genetic networks responsive to sodium butyrate in colonic epithelial cells

Genetic networks responsive to sodium butyrate in colonic epithelial cells

HLA-G gene repression is reversed by demethylation

Modulation of the Cyclin-Dependent Kinase Inhibitor p21WAF1/Cip1 Gene by Zac1 through the Antagonistic Regulators p53 and Histone Deacetylase 1 in HeLa Cells

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