Accession Number : AD1030558


Title :   Apoptosis Induction by Targeting Interferon Gamma Receptor 2 (IFNgammaR2) in Prostate Cancer: Ligand (IFNgamma) Independent Novel Function of IFNgammaR2 as a Bax Inhibitor


Descriptive Note : Technical Report,01 Aug 2012,31 Jul 2016


Corporate Author : Case Western Reserve University Cleveland United States


Personal Author(s) : Matsuyama,Shigemi


Full Text : https://apps.dtic.mil/dtic/tr/fulltext/u2/1030558.pdf


Report Date : 01 Oct 2016


Pagination or Media Count : 23


Abstract : 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).


Descriptors :   apoptosis , targeting , interferon , prostate cancer ligands , therapeutics , prostate , neoplasms , cell membrane , cell line


Distribution Statement : APPROVED FOR PUBLIC RELEASE