{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Ding XJ"],"funding":["Natural Science Foundation of Tianjin Municipality","National Natural Science Foundation of China","Tianjin Key Medical Discipline (Specialty) Construction Project"],"pagination":["e70028"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11868026"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["16(5)"],"pubmed_abstract":["<h4>Background</h4>Improving the \"cold\" tumor immune microenvironment (TIME) of small-cell lung cancer (SCLC) represents a promising therapeutic approach. The metabolite lactate plays a crucial role in shaping the immune-cold tumor microenvironment (TME) and facilitating tumor progression. Phosphoglycerate kinase 1 (PGK1) is a key enzyme involved in tumor lactate metabolism. This study demonstrates that ACT001 improves the TIME of SCLC through inhibiting lactate production by targeting PGK1.<h4>Methods</h4>The cytotoxic effects of ACT001 on SCLC cell lines NCI-H1688 and NCI-H446 were evaluated using MTT assay, clone formation, EdU incorporation, wound healing, and invasion assays. To elucidate the mechanism of action of ACT001, proteomic techniques, pull-down assays, LC-MS/MS, surface plas"],"journal":["Thoracic cancer"],"pubmed_title":["ACT001 Suppresses the Malignant Progression of Small-Cell Lung Cancer by Inhibiting Lactate Production and Promoting Anti-Tumor Immunity."],"pmcid":["PMC11868026"],"funding_grant_id":["82172635","21JCYBJC01000","82273794","TJYXZDXK-010A","82203628","82272686"],"pubmed_authors":["Wang WJ","Lu YX","Ding XJ","Qin TT","Huang DZ","Mei T","Chen Y","Xi XN","Wang JY"],"additional_accession":[]},"is_claimable":false,"name":"ACT001 Suppresses the Malignant Progression of Small-Cell Lung Cancer by Inhibiting Lactate Production and Promoting Anti-Tumor Immunity.","description":"<h4>Background</h4>Improving the \"cold\" tumor immune microenvironment (TIME) of small-cell lung cancer (SCLC) represents a promising therapeutic approach. The metabolite lactate plays a crucial role in shaping the immune-cold tumor microenvironment (TME) and facilitating tumor progression. Phosphoglycerate kinase 1 (PGK1) is a key enzyme involved in tumor lactate metabolism. This study demonstrates that ACT001 improves the TIME of SCLC through inhibiting lactate production by targeting PGK1.<h4>Methods</h4>The cytotoxic effects of ACT001 on SCLC cell lines NCI-H1688 and NCI-H446 were evaluated using MTT assay, clone formation, EdU incorporation, wound healing, and invasion assays. To elucidate the mechanism of action of ACT001, proteomic techniques, pull-down assays, LC-MS/MS, surface plas","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Mar","modification":"2025-04-22T20:07:57.092Z","creation":"2025-04-06T03:05:01.695Z"},"accession":"S-EPMC11868026","cross_references":{"pubmed":["40016971"],"doi":["10.1111/1759-7714.70028"]}}