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Methylselenium and Prostate Cancer Apoptosis

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The purpose of this research is to gain a better understanding of the biochemical pathways and molecular targets for the selective induction of apoptosis signaling and execution of prostate cancer PCa cells by methyl selenium Seselenol. We hypothesized that methyl selenium inhibits survival pathway leading to the activation of caspase-dependent apoptosis execution in PCa cells. The specific aims are to delineate the caspase-mediated execution pathways of apoptosis Objective 1 and to critically test the role of PISUB 3K-AKT survival pathway in apoptosis signaling Objective 2 induced by methyl Seselenol. We have performed experiments pertinent to these two objectives. Specifically, we established an inverse correlation between AKT activity and the sensitivity to MSeA in 3 PCa cell lines characterized the effects of PISUB 3K and AKT inhibitors as well as MEK-ERK inhibitor on MSeA -induced apoptosis established the caspase-dependence for apoptosis execution in LNCaP cells induced by MSeA when combined with inhibitors and showed greater impact on mitochondria cytochrome c release by PISUB 3K-AKT pathway than ERK established stable activated AKT transfectant DU145 clones and showed a AKT-dose-dependent increase in resistance to MSeA. Finally we also established the specificity of PIsub 3K-AKT and ERK regulation of MSeA induced death was not observed in selenite-induced death in LNCaP cells. These results have been published in Carcinogenesis, 2005 reprint.

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  • Biochemistry
  • Anatomy and Physiology

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