This article highlights some recent advances in
selenium cancer chemoprevention research. It has been well documented that the chemical transformation of
selenium to a monomethylated metabolite is an important step in achieving
cancer prevention. Studies with the rat mammary
carcinogenesis model suggested that
methylselenocysteine (MSC), a good precursor for generating
methylselenol endogenously, is able to block clonal expansion of premalignant lesions in the mammary gland. This finding supports the notion that
selenium intervenes at an early stage of
carcinogenesis. In addition to decreasing cell proliferation of the transformed colonies in vivo, MSC also enhances apoptosis. These same cellular responses are replicated with human premalignant breast cells grown in culture.
cDNA microarray analysis indicated that
selenium affects a multitude of molecular targets. Based on this information, a number of signaling pathways are proposed that could potentially provide insight into how
selenium might block cell cycle progression and induce cell death.