{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["9(21)"],"submitter":["Huang C"],"pubmed_abstract":["Immune checkpoint inhibitors targeting programmed cell death protein 1 (PD-1) or programmed cell death 1 ligand 1 (PD-L1) have enabled some patients with cancer to experience durable, complete treatment responses; however, reliable anti-PD-(L)1 treatment response biomarkers are lacking. Our research found that PD-L1 K162 was methylated by SETD7 and demethylated by LSD2. Furthermore, PD-L1 K162 methylation controlled the PD-1/PD-L1 interaction and obviously enhanced the suppression of T cell activity controlling cancer immune surveillance. We demonstrated that PD-L1 hypermethylation was the key mechanism for anti-PD-L1 therapy resistance, investigated that PD-L1 K162 methylation was a negative predictive marker for anti-PD-1 treatment in patients with non-small cell lung cancer, and showed "],"journal":["Science advances"],"pagination":["eade4186"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10219601"],"repository":["biostudies-literature"],"pubmed_title":["PD-L1 methylation restricts PD-L1/PD-1 interactions to control cancer immune surveillance."],"pmcid":["PMC10219601"],"pubmed_authors":["Chu Q","Huang C","Zheng X","Wu Q","Song D","Wang G","Jiang T","Zou C","Wang J","Jia K","Sun L","Hu F","Li Y","Hu J","Liu A","Chen Y","Luo X","Ren S","Lv P","Lan J"],"additional_accession":[]},"is_claimable":false,"name":"PD-L1 methylation restricts PD-L1/PD-1 interactions to control cancer immune surveillance.","description":"Immune checkpoint inhibitors targeting programmed cell death protein 1 (PD-1) or programmed cell death 1 ligand 1 (PD-L1) have enabled some patients with cancer to experience durable, complete treatment responses; however, reliable anti-PD-(L)1 treatment response biomarkers are lacking. Our research found that PD-L1 K162 was methylated by SETD7 and demethylated by LSD2. Furthermore, PD-L1 K162 methylation controlled the PD-1/PD-L1 interaction and obviously enhanced the suppression of T cell activity controlling cancer immune surveillance. We demonstrated that PD-L1 hypermethylation was the key mechanism for anti-PD-L1 therapy resistance, investigated that PD-L1 K162 methylation was a negative predictive marker for anti-PD-1 treatment in patients with non-small cell lung cancer, and showed ","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 May","modification":"2025-04-19T23:00:51.918Z","creation":"2025-04-19T23:00:51.918Z"},"accession":"S-EPMC10219601","cross_references":{"pubmed":["37235656"],"doi":["10.1126/sciadv.ade4186"]}}