Abstract

There is increasing evidence for the efficacy of certain forms of selenium (Se) as cancer‐chemopreventive compounds, and methylselenol has been hypothesized to be a critical selenium metabolite for anticancer activity in vivo. To determine differential chemopreventive effects of methylselenol on colon cancer cells versus normal colon cells, colon‐cancer‐derived HCT116 cells and nontumorigenic colon NCM460 cells were exposed to methylselenol. We found that submicromolar methylselenol exposure inhibited cell growth and led to an increase in the G1 and G2 fractions with a concomitant drop in the S‐phase. In addition, methylselenol inhibited the extracellular‐regulated kinase 1/2 (ERK1/2) signaling and c‐Myc expression. Importantly, methylselenol showed greater inhibition of cell growth, cell cycle, ERK1/2 signal and c‐Myc expression in colon‐cancer‐derived HCT116 cells, when compared to NCM460 colon cells. Similarly, submicromolar methylselenol induced a higher apoptosis rate in HCT116 cells (up to 3.2 fold of the control) than that in NCM460 colon cells (up to 1.4 fold of the control). Taken together, our data demonstrate that methylselenol's stronger potential of inhibiting colon cancer cell proliferation when compared with normal colon cells, which may be a critical mechanism by which selenium exerts its anticancer activity. Supported by USDA/ARS

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