Research Projects

Cancer cells undergo altered energy metabolism, leading to a surge in ATP requirement and metabolic stress. However, cancer cells alleviate this stress by elevating autophagy and shifting the metabolic preference from oxidative phosphorylation to aerobic glycolysis. This metabolic reprogramming can be a suitable therapeutic target in many cancer types. Enolase 1 (ENO1), a key glycolytic enzyme, can exert various cell functions depending on its sub-cellular localization. Epstein-Barr virus (EBV) is associated with 1% of total cancers worldwide, including several B-cell neoplasms. EBV infection transforms quiescent B-lymphocytes into hyper-proliferating B-cell blasts, establishing latency programs and differential expressions of viral oncoproteins. EBNA3C, a key viral oncoprotein required for efficient B-cell transformation, is typically expressed in latency III programs linked to immunoblastic lymphomas and in vitro generated lymphoblastoid cell lines (LCLs). Upon EBV infection, ENO1 transcript is significantly upregulated, likely regulated by coordinated actions of latent oncoprotein EBNALP, B-cell specific transcription factors cMyc and RUNX3, and histone super-enhancer mark H3K27ac. The role of ENO1 in regulating metabolic activities during EBV-induced B-cell lymphomagenesis is yet to be studied.