Selenium ablates Friend Virus induced Erythroleukemia in mice

Abstract

Selenium (Se), an essential micronutrient is reported to have anti‐inflammatory and anti‐tumorigenic properties. Recently, we have reported that anti‐inflammatory role of Se is mediated, in part, through the production of 15d‐PGJ2, a cyclopentanone prostaglandin D2 metabolite. Cyclopentanone prostaglandins, including 15d‐PGJ2, display anti‐inflammatory and anti‐proliferative properties. We hypothesize that Se acts through the production of 15d‐PGJ2 to mediate the anti‐carcinogenic effect by targeting cancer stem cells. In the current study, murine Friend‐virus (FVP) induced erythroleukemia model was used to examine the effect of Se and 15d‐PGJ2 on the ablation of spleen derived‐ leukemia stem cells (LSC), characterized by the expression of gp55, Sca, Kit, and Ter119. These cells retained the ability to proliferate in transplantation models and cause clonal leukemia. Infection of Balb/c mice fed on Se‐supplemented diets with FVP clearly protected the mice from splenomegaly; while those on Se‐deficient diet succumbed to infection. Furthermore, experiments with in‐vivo administration of 15d‐PGJ2 at physiologic doses also demonstrated a similar effect. Here we discuss the mechanisms of chemopreventive action of 15d‐PGJ2 and Se from the point of cancer stem cell apoptosis. NIH DK 077152Grant Funding Source: NIH