Submitted to: Federation of American Societies for Experimental Biology Conference
Publication Type: Abstract Only
Publication Acceptance Date: 11/2/2012
Publication Date: 4/9/2013
Citation: Zeng, H. 2013. Methylselenol, a selenium metabolite, inhibits colon cancer cell growth in vitro and in vivo. Federation of American Societies for Experimental Biology Conference. 27:860.13.
Technical Abstract: Methylselenol is hypothesized to be a critical selenium (Se) metabolite for anticancer activity. 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, and an induction of apoptosis in cancerous colon HCT116 cells, but to a much lesser extent in noncancerous NCM460 colon cells. The protein array analysis indicated that methylselenol changed the expression of 11 protein targets related to p53 tumor suppressor pathway via the regulation of cell cycle and apoptosis. Similarly, methylselenol inhibited the phosphorylation of extracellular-regulated kinase1/2 (ERK1/2) and p38 MAPK, and the expression of c-Myc in HCT116 cells, but also to a lesser extent in NCM460 cells, which may inhibit colon cancer cell proliferation. Consistent with these in vitro observations, the approach of either methylselenol-treated colon cancer cells or a daily single oral dose of methylselenol precursors (methylseleninic acid) greatly inhibits the growth of colon cancer xenografts in both Balb/C and C57/BL mouse models, respectively. Taken together, methylselenol’s strong potential of inhibiting colon cancer cell proliferation, may be an important mechanism by which selenium exerts its anticancer activity.