The effects of dietary selenomethionine on polyamines and azoxymethane-induced aberrant crypts

Baínes, Andrew D.; Holubec, Hanna; Basye, Jenny L.; Thorne, Patricia A.; Bhattacharyya, Achyut K.; Spallholz, Julian E.; Shriver, Brent J.; Cui, Haiyan; Roe, Denise J.; Clark, Larry; Earnest, David L.; Nelson, Mark A.

doi:10.1016/s0304-3835(00)00585-1

Cited by 26 publications

(15 citation statements)

References 14 publications

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“…A large body of experimental data, including animal models for colon cancer (42)(43)(44)(45), supports a role for selenium in cancer prevention (see for review, ref. 46), potentially acting through multiple pathways (47)(48)(49).…”

Section: Discussionmentioning

confidence: 99%

High Serum Selenium and Reduced Risk of Advanced Colorectal Adenoma in a Colorectal Cancer Early Detection Program

Peters

Chatterjee

Church

et al. 2006

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Background: Epidemiologic and animal studies suggest that selenium may reduce risk of colorectal cancer. However, the epidemiologic data is mainly from relatively small investigations, limiting their interpretation. Although substantial evidence suggests that smoking is a strong effect modifier for other antioxidative nutrients, little is known about smoking-selenium interactions in colorectal tumors. Methods: We studied the association of serum selenium and advanced colorectal adenoma, a cancer precursor, in 758 cases and 767 sex-and race-matched controls, randomly selected from the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. Cases had at least one verified advanced adenoma (z1 cm or villous elements, or high-grade dysplasia) of the distal colon, and controls had a negative sigmoidoscopy.

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Section: Discussionmentioning

confidence: 99%

High Serum Selenium and Reduced Risk of Advanced Colorectal Adenoma in a Colorectal Cancer Early Detection Program

Peters

Chatterjee

Church

et al. 2006

Cancer Epidemiology, Biomarkers &Amp; Prevention

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“…Dietary SeMet supplementation of 2 p.p.m. resulted in a marked reduction of the number of aberrant crypt foci in an azoxymethane-induced model (Baines et al, 2000).…”

Section: Selenium Compoundsmentioning

confidence: 97%

Selenomethionine induction of DNA repair response in human fibroblasts

2002

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Selenium compounds have a long history in chemoprevention of mammary and colon cancers in rodent models. Selenium compounds are in current clinical trials, having shown promise in prevention of prostate and other human cancers. In human tissues, it has been estimated that each cell sustains approximately 10 000 potentially mutagenic (if not repaired) lesions per day due to endogenous DNA damage. Almost no studies have addressed the potential for selenium compounds to induce DNA repair, a potential mechanism for their cancer-preventive actions. We show that selenium in the form of selenomethionine induces a DNA repair response in normal human ®broblasts in vitro, and protects cells from DNA damage. We show a possible mechanism for the inducible DNA repair response, in which enhanced repair complex formation was observed in selenomethionine-treated cells.

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“…[11][12][13][14][15][16] SeMet has been shown to inhibit cell growth through its effect on the cell cycle in several model systems. SeMet can increase the percentage of cells in the G 2 /M phase in colon cancer cells when used at a low dose 17 and in prostate cancer cells at a very high dose (500 mM).…”

Section: Introductionmentioning

confidence: 99%

Profiling of selenomethionine responsive genes in colon cancer by microarray analysis

Goulet¹,

Watts²,

Lord³

et al. 2007

Cancer Biology & Therapy

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AbbreviAtioNs AbstrACtHigh-selenium containing yeast is being evaluated in clinical trials against colon polyp recurrence. However, the molecular targets for the anticancer effects of selenium remain unclear. Previous studies by our group demonstrated that selenomethionine-induced growth arrest appears to be mediated by activation of ERK and subsequent phosphorylation of RSK and histone H3. These results suggest that selenomethionine can alter gene expression. In the present study, we have used cDNA microarrays to determine whether gene expression differences exist in HCT116 colon cancer cells treated with selenomethionine. These experiments reveal statistically significant expression changes for 50 genes. Genes we found to increase with selenomethionine treatment include KLK6, ATOX1, SGK, GJB2, DAP-1, PLAU, VIM, DPYSL2, STC2 and PXN. Conversely, genes downregulated by selenomethionine include PRKACB, LIM, DEPP, MYC, CDH5, ELF3, VSNL1, SAT and EGLN3. Further analysis of those genes using chromatin immunoprecipitation experiments showed that phosphorylated histone H3 on serine 10 bound to the GJB2 promoter (connexin 26) or the serum glucocorticoid kinase promoter is increased with selenomethionine treatment. Cells overexpressing CX26 or DAP-1 displayed a reduced number of colonies which suggests that these two genes could play a functional role in the growth inhibitory effects of selenomethionine. These data support the notion that selenomethionine-induced growth inhibition is associated with global changes in gene expression. They also demonstrate that selenomethionine can modify chromatin state to alter gene transcription. Finally, our studies provide a practical foundation for the further development of biomarkers to monitor the efficacy of selenomethionine in clinical trials.

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The effects of dietary selenomethionine on polyamines and azoxymethane-induced aberrant crypts

Cited by 26 publications

References 14 publications

High Serum Selenium and Reduced Risk of Advanced Colorectal Adenoma in a Colorectal Cancer Early Detection Program

High Serum Selenium and Reduced Risk of Advanced Colorectal Adenoma in a Colorectal Cancer Early Detection Program

Selenomethionine induction of DNA repair response in human fibroblasts

Profiling of selenomethionine responsive genes in colon cancer by microarray analysis

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