{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Wu Z"],"funding":["National Natural Science Foundation of China"],"pagination":["e155224"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8970670"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["132(7)"],"pubmed_abstract":["The functional integrity of CD8+ T cells is tightly coupled to metabolic reprogramming, but how oxidative stress directs CD8+ T cell metabolic fitness in the tumor microenvironment (TME) remains elusive. Here, we report that SUMO-specific protease 7 (SENP7) senses oxidative stress to maintain the CD8+ T cell metabolic state and antitumor functions. SENP7-deficient CD8+ T cells exhibited decreased glycolysis and oxidative phosphorylation, resulting in attenuated proliferation in vitro and dampened antitumor functions in vivo. Mechanistically, CD8+ T cell-derived ROS triggered cytosolic SENP7-mediated PTEN deSUMOylation, thereby promoting PTEN degradation and preventing PTEN-dependent metabolic defects. Importantly, lowering T cell-intrinsic ROS restricted SENP7 cytosolic translocation and r"],"journal":["The Journal of clinical investigation"],"pubmed_title":["SENP7 senses oxidative stress to sustain metabolic fitness and antitumor functions of CD8+ T cells."],"pmcid":["PMC8970670"],"funding_grant_id":["81930040,31922025,32170908"],"pubmed_authors":["Wu Z","Han Q","Ding R","Hu Z","Zhao R","Huang H","Teng XL","Zou Q","Ye Y","Wang Z","Yu X"],"additional_accession":[]},"is_claimable":false,"name":"SENP7 senses oxidative stress to sustain metabolic fitness and antitumor functions of CD8+ T cells.","description":"The functional integrity of CD8+ T cells is tightly coupled to metabolic reprogramming, but how oxidative stress directs CD8+ T cell metabolic fitness in the tumor microenvironment (TME) remains elusive. Here, we report that SUMO-specific protease 7 (SENP7) senses oxidative stress to maintain the CD8+ T cell metabolic state and antitumor functions. SENP7-deficient CD8+ T cells exhibited decreased glycolysis and oxidative phosphorylation, resulting in attenuated proliferation in vitro and dampened antitumor functions in vivo. Mechanistically, CD8+ T cell-derived ROS triggered cytosolic SENP7-mediated PTEN deSUMOylation, thereby promoting PTEN degradation and preventing PTEN-dependent metabolic defects. Importantly, lowering T cell-intrinsic ROS restricted SENP7 cytosolic translocation and r","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Apr","modification":"2026-05-31T06:02:01.86Z","creation":"2025-02-19T01:54:56.715Z"},"accession":"S-EPMC8970670","cross_references":{"pubmed":["35143421"],"doi":["10.1172/JCI155224"]}}