Apoptosis Induction by Targeting Interferon Gamma Receptor 2 (IFNgammaR2) in Prostate Cancer: Ligand (IFNgamma) Independent Novel Function of IFNgammaR2 as a Bax Inhibitor
Technical Report,01 Aug 2012,31 Jul 2016
Case Western Reserve University Cleveland United States
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In our preliminary study, we found that IFNR2 has previously unknown function as an inhibitor of Bax. Bax isa key mediator of apoptosis. We found that IFNR2 is overexpressed in prostate cancer, and we hypothesize that abnormally high level of IFNR2 confers apoptosis resistance of prostate cancer. In this project, we accomplished the following three tasks. Task1 Search for the binding domains of IFNR2 and Bax. Our experiments suggest that Bax binding domain mayexists in amino acid 301-308 of IFNR2, and that IFNR2 does not require the N-terminal 53 amino acids of Bax. Task2 Identification of IFNR2 expressing PCa We found that basal cell, but not luminal cell, of prostate tissue of prostate cancer patients expressed high level of IFNR2. We also found that IFNR2 expression level increases according to the progression of malignancy in cell lines from androgen-dependent, androgen-independent, and bone metastatic.