Abstract 4757: TNFAIP8 facilitates metabolic reprogramming in prostate cancer cells

Abstract

Abstract Tumor necrosis factor-α-induced protein 8 (TNFAIP8), a member of TIPE/TNFAIP8 family, has been associated with multiple oncogenic roles in human cancers. Here we investigated the role of TNFAIP8 in metabolic reprogramming in prostate cancer (PCa) cells. Ectopic expression of TNFAIP8 increased cell survival/proliferation by enhancing metabolic activity in PCa cells. TNFAIP8 activated the PI3K-AKT pathway and up-regulated the expression of cell proliferation markers, cell cycle-related proteins, and PCa stem cell markers. TNFAIP8 was also found to regulate the expression of glucose metabolizing enzymes, enhancing glucose consumption, and endogenous ATP production. Treatment with glycolysis inhibitor 2-deoxyglucose (2-DG) reduced TNFAIP8 mediated glucose consumption /ATP production and spheroid formation in PCa cells. Moreover, TNFAIP8 maintained mitochondrial membrane potential and increased glycolysis/oxidative phosphorylation. These changes were also consistent with an observed altered metabolomic profile in PCa cells transfected with TNFAIP8. Collectedly, our data suggest that TNFAIP8 exerts its oncogenic effects by enhancing glucose metabolism and by facilitating metabolic reprogramming in PCa cells. Citation Format: Suryakant Niture, Minghui Lin, Joab O. Odera, John Moore, Deepak Kumar. TNFAIP8 facilitates metabolic reprogramming in prostate cancer cells [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr 4757.