Abstract
We review recent data that support a potential antiangiogenic effect of selenium (Se) in the chemoprevention of cancer and data that contrast two pools of Se metabolites, namely, methylselenol vs. hydrogen selenide, that differentially affect proteins and cellular processes crucial to tumor angiogenesis regulation. With regard to tumor angiogenesis, the chemopreventive effect of increased Se intake on chemically induced mammary carcinogenesis has been associated with reduced intratumoral microvessel density and an inhibition of the expression of vascular endothelial growth factor. The in vitro data show that monomethyl Se potently inhibits cell cycle progression of vascular endothelial cells to the S phase, endothelial expression of matrix metalloproteinase-2, and cancer epithelial expression of vascular endothelial growth factor with concentrations giving half-maximal inhibition that are within the plasma range of Se in US adults. The methyl Se-specific activities may therefore be physiologically pertine...