Affiliations: United States Department of Agriculture, Agricultural
Research Service, Grand Forks Human Nutrition Research Center, Grand Forks, ND,
USA
Note: [] Address for correspondence: Huawei Zeng, Ph.D., USDA, ARS,
GFHNRC, P. O. Box 9034, Grand Forks, ND 58202-9034, USA. Tel.: +1 701 795 8465;
Fax: +1 701 795 8220; E-mail: huawei.zeng@ars.usda.gov
Abstract: Selenium (Se) is a potential anticarcinogenic nutrient, and the
essential role of Se in cell growth is well recognized but certain cancer cells
appear to have acquired a survival advantage under conditions of Se-deficiency.
To understand the molecular basis of Se-anticancer effects at nutritional doses
(nmol/L) for cultured cells, we generated Se-deficient colon Caco-2 cells by
gradually reducing serum in media because serum contains a trace amount of Se.
The glutathione peroxidase (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, SeMSC or SeMet (three
tested Se-chemical forms) after 7-d culture in serum free media. Interestingly,
there were no detectable differences in cell growth, cell cycle progression
between Se-deficient cells and cells supplemented with 500 nmol/L Se. To
examine differential cancer signaling-gene expression between Se-deficient and
Se-supplemented cells, we employed a cancer signal pathway-specific array assay
coupled with the real time PCR analysis. Our data demonstrate that although
Caco-2 cells are resistant to Se deprivation, Se may exert its anticancer
property through increasing the expression of humoral defense gene (A2M) and
tumor suppressor-related genes (IGFBP3, HHIP) while decreasing pro-inflammatory
gene (CXC L9, HSPB2) expression.
