Submitted to: Journal of Federation of American Societies for Experimental Biology
Publication Type: Abstract Only
Publication Acceptance Date: 2/4/2008
Publication Date: 4/15/2008
Publication URL: www.fasebj.org
Citation: Zeng, H., Botnen, J.H. 2008. Selenium is critical for the regulation of tumor suppressor and pro-inflammatory gene expresssion in human colon Caco-2 cells. [abstract] Journal of Federation of American Societies for Experimental Biology. 22:696.2. Interpretive Summary:
Technical Abstract: The essential role of Se in growth of most mammalian cells is well recognized but certain cancer cells appear to have acquired a survival advantage under conditions of Se-deficiency. We generated Se-deficient colon Caco-2 cells by gradually reducing serum in the media because serum contains a trace amount of Se, which is sufficient to maintain the expression of cellular selenoproteins such as glutathione peroxidase (GPx). The GPx activity of Se-deficient Caco-2 cells was 10.8 mU/mg protein compared to 133.6~146.3 mU/mg protein in Caco-2 cells supplemented with 500 nmol/L selenite, Se- (methyl)selenocysteine or selenomethionine (three tested Se chemical forms) after 7- day culture in serum free media. Interestingly, there were not detectable differences on cell growth, cell cycle progression between Se-deficient and Se-supplemented cells. However, cancer signal pathway-specific array assay and the real time PCR analysis demonstrated that Se increased the expression of humoral defense gene (A2M) and tumor suppressor-related genes (IGFBP3, HHIP) but decreased pro-inflammatory gene (CXC L9, HSPB2) expression at cellular nutritional Se doses, even though colon Caco-2 cells were resistant to Se deprivation.