Induction and superinduction of growth arrest and DNA damage gene 45 (GADD45) α and β messenger RNAs by histone deacetylase inhibitors trichostatin A (TSA) and butyrate in SW620 human colon carcinoma cells

Chen, Zunxuan; Clark, Steven C.; Birkeland, Marian L.; Sung, Chiu Mei; Lago, Amparo; Liu, Ronggang; Kirkpatrick, Robert B.; Johanson, Kyung; Winkler, James D.; Hu, Erding

doi:10.1016/s0304-3835(02)00322-1

Cited by 86 publications

(62 citation statements)

References 65 publications

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“…In addition, because we observed a dramatic effect of HDACi on cell viability that seems to depend more on the exposure conditions than inhibitor selectivity, we asked whether the expression of genes involved in the regulation of the cell cycle would be affected by HDACi according to the treatment regimen and not based on their selectivity profile. Previous studies showed that enhanced histone acetylation induced by HDACi allowed the overexpression of genes involved in cell cycle arrest such as cyclin-dependent kinase inhibitors or the growth arrest and DNA damage-inducible protein GADD45 gene family (11,28,40,(45)(46)(47)(48)(49). Our Gene Ontology analysis revealed that the cyclin-dependent kinase activity pathway was up-regulated by a 24-h constant exposure to SAHA and C1.…”

Section: Discussionmentioning

confidence: 99%

Histone Deacetylase (HDAC) Inhibitor Kinetic Rate Constants Correlate with Cellular Histone Acetylation but Not Transcription and Cell Viability

Lauffer

Mintzer²,

Fong³

et al. 2013

Journal of Biological Chemistry

346

352

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Background:The effect of HDAC inhibitor kinetic properties on biological function is currently unknown. Results:The kinetic rate constants of HDAC inhibitors differentially affect histone acetylation, cell viability, and gene expression. Conclusion: Evaluating HDAC inhibitor properties using histone acetylation is not predictive of their function on cellular activity. Significance: Characterizing the biological effect of different HDAC inhibitors will help to evaluate their clinical utility.

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Section: Discussionmentioning

confidence: 99%

Histone Deacetylase (HDAC) Inhibitor Kinetic Rate Constants Correlate with Cellular Histone Acetylation but Not Transcription and Cell Viability

Lauffer

Mintzer²,

Fong³

et al. 2013

Journal of Biological Chemistry

346

352

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“…In some instances, HDACIs repress gene expression by an indirect mechanism that involves recruitment of a repressor protein rather than a transcriptional activator as a consequence of histone acetylation. [3][4][5][6][7][8][9][76][77][78] Treatment with HDACIs was found to repress the expression of cyclin D1, cyclin A, Bcl-2, vascular endothelial growth factor (VEGF) and hypoxia inducible factor (HIF)-1α. Besides histone acetylation, treatment with HDACIs was found to result in hyperacetylation of numerous non-histone proteins that are required for transcription, cell cycle, signal transduction, and other cellular functions.…”

Section: Anti-tumor Activity Of Hdacismentioning

confidence: 99%

Histone Deacetylase Inhibitors for Cancer Therapy

Kim¹,

Bang²,

Robertson³

2006

Epigenetics

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The epigenome of cancer cells is determined by DNA methylation and an array of post-translational modifications of the core histones. Epigenetic abnormalities are commonly found in human tumors and importantly, they can be reversed by pharmacologic inhibitors. Histone deacetylase inhibitors (HDACIs) represent one of the most promising epigenetic treatments for cancer. HDACIs have emerged as promising targets for cancer therapy because they reactivate the transcription of multiple genes that are silenced in human tumors and they show pleiotropic anti-tumor effects selectively in cancer cells. HDACIs are well-tolerated and several show promising anti-tumor activity. While gene transcription has been considered to be the major target of HDACIs, inhibition of acetylation of non-histone proteins is now emerging as a novel basis for their anti-tumor effects. In this review, we discuss new insights into the molecular mechanism of HDACIs, their current status of clinical development, and possible future uses in cancer therapy.

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“…Mutation of individual Oct or NF-Y sites in the murine GADD45g promoter did not hamper its activation by TSA, suggesting that either site is sufficient to mediate activation by TSA. This inhibitor has been previously shown to upregulate GADD45a mRNA levels in human colon carcinoma and osteosarcoma cells (Della-Ragione et al, 2001;Chen et al, 2002;Hirose et al, 2003) and GADD45b mRNA levels in human colon carcinoma cells (Chen et al, 2002). Because we have not directly investigated whether GADD45a or GADD45b expression is induced by TSA in NIH3T3 cells, we cannot rule out that this inhibitor might also induce the expression of these genes in NIH3T3 or Jurkat cells.…”

Section: Discussionmentioning

confidence: 94%

“…HDAC inhibitors, such as trichostatin A (TSA; Sigma, Tres Cantos, Madrid, Spain), induce many genes coding for proteins involved in cell cycle control, including GADD45a and GADD45b (Della-Ragione et al, 2001;Chen et al, 2002;Hirose et al, 2003), and stop tumor growth by eliciting either cell cycle arrest or apoptosis in tumor cells (Johnstone, 2002).…”

Section: Introductionmentioning

confidence: 99%

The histone deacetylase inhibitor trichostatin A induces GADD45γ expression via Oct and NF-Y binding sites

2007

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The GADD45c protein is a potential tumor suppressor whose expression is reduced in several tumors. However, very little is known about the regulation of its expression. We have determined that the most relevant region of its promoter lies between nucleotides À112 and À54, relative to the transcription start site. Putative Oct and NF-Y elements were found in this region and factors belonging to these families interacted with these elements in vitro and with the promoter in vivo. Mutation of these elements reduced the basal activity of the promoter, suggesting that both sites are essential for basal expression. These factors interact with chromatin modifying proteins and we found that histone deacetylase 1 or silencing mediator for retinoid and thyroid hormone receptor overexpression reduced the basal activity of the promoter. In contrast, forced expression of the histone acetylase protein PCAF or cell treatment with the HDAC inhibitor trichostatin A increased GADD45c mRNA levels and induced GADD45c promoter activity through its Oct and NF-Y elements. Moreover, ectopic expression of a dominantnegative version of NF-YA strongly inhibited trichostatin A-induced activation of the promoter. Our data strongly suggest that inhibition of deacetylase activity could potentially be used for treatment of tumors where GADD45c expression is reduced.

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Induction and superinduction of growth arrest and DNA damage gene 45 (GADD45) α and β messenger RNAs by histone deacetylase inhibitors trichostatin A (TSA) and butyrate in SW620 human colon carcinoma cells

Cited by 86 publications

References 65 publications

Histone Deacetylase (HDAC) Inhibitor Kinetic Rate Constants Correlate with Cellular Histone Acetylation but Not Transcription and Cell Viability

Histone Deacetylase (HDAC) Inhibitor Kinetic Rate Constants Correlate with Cellular Histone Acetylation but Not Transcription and Cell Viability

Histone Deacetylase Inhibitors for Cancer Therapy

The histone deacetylase inhibitor trichostatin A induces GADD45γ expression via Oct and NF-Y binding sites

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