{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Yan L"],"funding":["Open Research Project of the Key Laboratory of Viral Pathogenesis & Infection Prevention and Control of the Ministry of Education","the Outstanding Innovative Talents Cultivation Funded Programs for Doctoral Students of Jinan University","the Science and Technology Project of Heyuan, China Social Development and Rural Science","the Project of Guangdong Administration of Traditional Chinese Medicine","the Natural Science Foundation of Guangdong Province","the National Natural Science Foundation of China","Medical Joint Fund of Jinan University"],"pagination":["1001"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12461981"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["23(1)"],"pubmed_abstract":["Background
Metabolic reprogramming is a hallmark of cancer cells, enabling them to meet the heightened energetic and biosynthetic demands required for rapid growth and proliferation. Recently, non-canonical functions of metabolic enzymes have garnered significant attention in cancer research. Pyruvate kinase 2 (PKM2) has been identified as a key player in transcriptional regulation within the nucleus, presenting new opportunities for therapeutic interventions in cancer.Methods
In this study, the cells (A549 and H1299) were treated with indicator concentration of triclabendazole. The effects of triclabendazole on proliferation was detected by CCK8 assay, colony formation assay, EdU staining, and cell count assay. A tumorigenesis study in nude mice was performed to demonstrat"],"journal":["Journal of translational medicine"],"pubmed_title":["Triclabendazole inhibits PKM2 nuclear localization and glycolysis by enhancing HDAC6-mediated deacetylation in lung cancer."],"pmcid":["PMC12461981"],"funding_grant_id":["20232177","2024VPPC-R01","2023008","2021CXB023","82274167","2023A1515010578","YXJC2024006"],"pubmed_authors":["Shi SS","Yan L","Qu LZ","Li Y","Liu J","Zhang YF","Zha QB","Fan J","Sun Y","Dai Y"],"additional_accession":[]},"is_claimable":false,"name":"Triclabendazole inhibits PKM2 nuclear localization and glycolysis by enhancing HDAC6-mediated deacetylation in lung cancer.","description":"Background
Metabolic reprogramming is a hallmark of cancer cells, enabling them to meet the heightened energetic and biosynthetic demands required for rapid growth and proliferation. Recently, non-canonical functions of metabolic enzymes have garnered significant attention in cancer research. Pyruvate kinase 2 (PKM2) has been identified as a key player in transcriptional regulation within the nucleus, presenting new opportunities for therapeutic interventions in cancer.Methods
In this study, the cells (A549 and H1299) were treated with indicator concentration of triclabendazole. The effects of triclabendazole on proliferation was detected by CCK8 assay, colony formation assay, EdU staining, and cell count assay. A tumorigenesis study in nude mice was performed to demonstrat","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Sep","modification":"2026-06-03T20:28:07.874Z","creation":"2026-06-01T03:06:23.462Z"},"accession":"S-EPMC12461981","cross_references":{"pubmed":["40993625"],"doi":["10.1186/s12967-025-06905-5"]}}