Selenium is an essential
micronutrient for humans and animals, and is thought to provide protection against some forms of
cancer. These protective effects appear to be mediated, at least in part, through
selenium-containing
proteins (
selenoproteins). Recent studies in a mouse
colon cancer cell line have shown that the 15 kDa
selenoprotein (Sep15) may also play a role in promoting
colon cancer. The current study investigated whether the effects of reversing the
cancer phenotype observed when Sep15 was removed in mouse
colon cancer cells, were recapitulated in HCT116 and HT29 human
colorectal carcinoma cells. Targeted down-regulation of Sep15 using RNAi technology in these human
colon cancer cell lines resulted in similarly decreased growth under anchorage-dependent and anchorage-independent conditions. However, the magnitude of reduction in cell growth was much less than in the mouse
colon cancer cell line investigated previously. Furthermore, changes in cell cycle distribution were observed, indicating a delayed release of Sep15 deficient cells from the G(0)/G(1) phase after synchronization. The potential mechanism by which human
colon cancer cells lacking Sep15 revert their
cancer phenotype will need to be explored further.