Regulation of the rat metallothionein-I gene by sodium butyrate

Birren, Bruce W.; Herschman, Harvey R.

doi:10.1093/nar/14.2.853

Cited by 50 publications

(18 citation statements)

References 45 publications

(50 reference statements)

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“…metallothionein-1 genes in nonintestinal cells (45,46). Butyrate does not apparently downregulate CFTR in HT29 cells; in fact, CFTR mRNA is induced by butyrate, although this increase occurs without a corresponding increase in cAMPdependent Cl Ϫ channel function.…”

Section: Discussionmentioning

confidence: 89%

Na-K-2Cl cotransporter gene expression and function during enterocyte differentiation. Modulation of Cl- secretory capacity by butyrate.

Matthews

Hassan²,

Meng³

et al. 1998

J. Clin. Invest.

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Section: Discussionmentioning

confidence: 89%

Na-K-2Cl cotransporter gene expression and function during enterocyte differentiation. Modulation of Cl- secretory capacity by butyrate.

Matthews

Hassan²,

Meng³

et al. 1998

J. Clin. Invest.

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“…For instance, this protein was overexpressed in bladder cancer but down-regulated in advanced prostate cancer (32,33). Although other metallothioneins have been found to be up-regulated by butyrate in a paradigm of increased resistance to toxic metals in tetracarcinoma and hepatoma cells (34,35), this is the first report on the regulation of metallothioneins by butyrate in colorectal cancer cells. Metallothioneins have a high metal binding affinity for metal homeostasis and detoxification.…”

Section: Cluster B: Apoptosismentioning

confidence: 87%

Quantitative and Temporal Proteome Analysis of Butyrate-treated Colorectal Cancer Cells

Tan¹,

Tan

Lin

et al. 2008

Molecular & Cellular Proteomics

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Colorectal cancer is one of the most common cancers in developed countries, and its incidence is negatively associated with high dietary fiber intake. Butyrate, a shortchain fatty acid fermentation by-product of fiber induces cell maturation with the promotion of growth arrest, differentiation, and/or apoptosis of cancer cells. The stimulation of cell maturation by butyrate in colonic cancer cells follows a temporal progression from the early phase of growth arrest to the activation of apoptotic cascades. Previously we performed two-dimensional DIGE to identify differentially expressed proteins induced by 24-h butyrate treatment of HCT-116 colorectal cancer cells. Herein we used quantitative proteomics approaches using iTRAQ (isobaric tags for relative and absolute quantitation), a stable isotope labeling methodology that enables multiplexing of four samples, for a temporal study of HCT-116 cells treated with butyrate. In addition, cleavable ICAT, which selectively tags cysteine-containing proteins, was also used, and the results complemented those obtained from the iTRAQ strategy. Selected protein targets were validated by real time PCR and Western blotting. A model is proposed to illustrate our findings from this temporal analysis of the butyrateresponsive proteome that uncovered several integrated cellular processes and pathways involved in growth arrest, apoptosis, and metastasis. These signature clusters of butyrate-regulated pathways are potential targets for novel chemopreventive and therapeutic drugs for treatment of colorectal cancer. Molecular & Cellular Proteomics 7:1174 -1185, 2008.In developed countries, colorectal cancer is a prevalent disease with high mortality and morbidity rates (1). This disease has emerged as the top malignancy in Singapore. Environmental factors are responsible for about 80% of the cases, whereas genetic predisposition accounts for the minority 20% of cases. Epidemiological evidence suggests that high intake of dietary fiber reduces the incidence and risk of this neoplasm (2, 3). A wealth of studies has shown that butyrate produced from anaerobic fermentation of indigestible carbohydrate is the molecule responsible for the chemopreventive properties of a fiber-rich diet (4 -6).Although butyrate serves as an energy source for normal colonocytes, in vivo and in vitro studies have shown that at physiological concentrations this natural short-chain fatty acid mediates cell maturation with the promotion of growth arrest followed by differentiation and/or apoptosis of cancer cells (7-11). These biological effects are crucial in colorectal cancer therapy as colonic transformation is characterized by multistage alterations of tissue homeostasis resulting in aberrant cell division and/or cell death (12, 13). Butyrate has been purported as a potential anticancer agent. This initiated notable research in identifying proteins that contribute to its biological effects (14, 15). However, most of these investigations focused on one target at any one time and were thus unable to systematica...

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“…3). Cd produces a more rapid and a greater overall MT-I mRNA induction than does butyrate (4). Hypersensitivity studies show that Cd2+ induces substantial alterations in chromatin containing the MT-I gene (36).…”

mentioning

confidence: 94%

“…Butyrate acts additively with dexamethasone (an inducer of the MT-I gene) in stimulating MT-I message levels in H4IIE cells (4). Like the MT-I gene, the tyrosine aminotransferase (TAT) gene is expressed in H4IIE cells and is induced by glucocorticoid hormones.…”

mentioning

confidence: 99%

Butyrate-induced changes in nuclease sensitivity of chromatin cannot be correlated with transcriptional activation.

1987

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We examined in the H4IIE rat hepatoma cell line the relationship between butyrate-induced changes in the nuclease sensitivity of chromatin and changes in transcriptional activity of specific genes. The butyrate-inducible metallothionein I (MT-I) gene underwent a dramatic increase in DNase I sensitivity after 3 h of butyrate treatment. However, genes not transcribed in H4IIE cells underwent the same changes in DNase I sensitivity. Thus, butyrate-induced increases in DNase I sensitivity are not sufficient for the transcriptional activation of a gene. Butyrate treatment has also been reported to alter the sensitivity of sequences to micrococcal nuclease (MNase) in a manner reflecting their tissue-specific expression. Butyrate exposure caused increased digestion of the MT-I gene by MNase. However, butyrate-induced MNase sensitivity also occurred for genes which are neither transcribed in untreated cells nor butyrate inducible. Moreover, cadmium, a potent transcriptional activator of the MT-I gene, does not alter the sensitivity of the MT-I gene to MNase. Thus, the butyrate-induced alterations in MNase sensitivity are neither sufficient for, necessary for, nor indicative of transcriptional activation.

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Regulation of the rat metallothionein-I gene by sodium butyrate

Cited by 50 publications

References 45 publications

Na-K-2Cl cotransporter gene expression and function during enterocyte differentiation. Modulation of Cl- secretory capacity by butyrate.

Na-K-2Cl cotransporter gene expression and function during enterocyte differentiation. Modulation of Cl- secretory capacity by butyrate.

Quantitative and Temporal Proteome Analysis of Butyrate-treated Colorectal Cancer Cells

Butyrate-induced changes in nuclease sensitivity of chromatin cannot be correlated with transcriptional activation.

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