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ARS Home » Plains Area » Grand Forks, North Dakota » Grand Forks Human Nutrition Research Center » Dietary Prevention of Obesity-related Disease Research » Research » Publications at this Location » Publication #221507
Title: Molecular mechanisms of cancer prevention by selenium

Author
item Zeng, Huawei

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 2/20/2008
Publication Date: 7/15/2008
Citation: Zeng, H. 2008. Molecular mechanisms of cancer prevention by selenium. [abstract]. BIT Life Sciences' 1st World Cancer Congress. p. 365.

Interpretive Summary:

Technical Abstract: Selenium (Se) is an essential dietary component for animals including humans, and there is increasing evidence for the efficacy of certain forms of selenium as cancer-chemopreventive compounds. In addition, Se appears to have a protective effect at various stages of carcinogenesis including both the early and later stages of cancer progression. Mechanisms for Se-anticancer action are not fully understood, however, several have been proposed: antioxidant protection, enhanced carcinogen detoxification, enhanced immune surveillance, modulation of cell proliferation (cell cycle and apoptosis), inhibition of tumor cell invasion, and inhibition of angiogenesis. Cell-cycle analysis revealed that Se deficiency caused a decrease in G1 Phase cells that corresponded to an increase in G2 and sub-G1 phase cells. Our gene array data indicated that c-Myc, cyclin C, proliferating cell nuclear antigen, cyclin-dependent kinase (cdk)1, cdk2, cdk4, cyclin B and cyclin D2 mRNA levels were lower in Se-deficient cells than in the cells supplemented with 0.25 umol/L selenomethionine (a cellular nutritional dose). These genes are critical for the cell cycle progression, particularly G2/M transition and /or the reduction of apoptosis. At supranutritional levels, methylselenol has been hypothesized to be a critical Se metabolite for anticancer activity in vivo. In subsequent studies, we have shown that methylselenol increases the expression of both pro-metastatic genes, MMP-2 and MMP-9, and anti-metastatic genes, TIMP-1 and TIMP-2. The net effect of these increases is the inhibition of pro-MMP-2 activation and of tumor cell migration and invasion capacity. Collectively, these data demonstrate that Se modulates cell proliferation and inhibits tumor cell invasion.