Glutathione S-transferase A2 promotes hepatocellular carcinoma recurrence after liver transplantation through modulating reactive oxygen species metabolism

Abstract Hepatocellular carcinoma (HCC) recurrence after liver transplantation remains a significant clinical problem. Ischemia-reperfusion injury (IRI) occurred inevitably at the early phase (LT) spawns risk of HCC recurrence. However, their linkage and IRI-derived factors for remain exclusive. Understanding mechanism post-transplantation hepatic could provide new strategies to prevent later event We demonstrated that glutathione S-transferase A2 (GSTA2) expression was significantly associated with systemic ROS level transplantation. Early circulating GSTA2 ( EPC GSTA2) protein predictor survival. Heterogeneous single nucleotide polymorphism G335C poor survival recipients. Enhancement protect cells against H 2 O -induced cell death by compensating elevated stress. also played crucial roles in regulating ROS-associated JNK AKT signaling pathways metabolism HCCs responding dynamic environment. Functionally, endogenous or exogenous upregulation promote growth invasion through activating epithelial–mesenchymal-transition process. Targeted inhibition suppress metastasis. In conclusion, be novel prognostic therapeutic target combat