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

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Technical Report,01 Aug 2014,31 Jul 2015

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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 is a 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 will investigate the role of IFNR2 in drug resistance of prostate cancer and explore the development of strategies that can activate Bax-induced apoptosis in prostate cancer by inactivating IFNR2. In Year 3, we planned to determine what kind of cell types in prostate cancer tissue expresses IFNR2 by performing immunohistochemistry. Another important proposed experiment is to determine whether IFNR2 expression profile expression levels and expression type cytosol or membrane expression, or cell type specific staining can be used as a biomarker to predict the clinical outcome. In this report, we show that IFNR2 is expressed in a particular group of basal cells in prostate of patients who had recurrence. IFNR2 positive cells were not detected in luminal cells or luminal cell type cancer cells. Using prostate cancer cell lines, we found that IFNR2 expression increases according to the progression of malignancy, i.e. from androgen-dependent state to androgen-independent and metastatic state. These results suggest that elevation of IFNR2 expression is correlated with progression of prostate cancer.

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