{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["15"],"submitter":["Li G"],"pubmed_abstract":["<h4>Background</h4>Gliomas, particularly glioblastoma, are aggressive brain tumors with poor prognosis and unmet therapeutic needs. Structural maintenance of chromosomes 4 (SMC4), a core component of the condensin complex, is dysregulated in multiple cancers, but its role in glioma metabolism and metastasis remains unclear.<h4>Methods</h4>Using integrated multi-omics analyses of glioma datasets, we assessed SMC4 expression and its correlation with clinical outcomes. Functional studies in U-251MG and LN229 glioma cells including CCK-8, EdU, cell cycle, Transwell, and wound-healing assays were combined with subcutaneous xenograft and tail-vein metastasis mouse models to evaluate SMC4's effects on proliferation, migration, invasion, and metastasis. ECAR/OCR and rescue experiments validated SM"],"journal":["Frontiers in oncology"],"pagination":["1624370"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12417569"],"repository":["biostudies-literature"],"pubmed_title":["NFIA-dependent upregulation of SMC4 promotes metastasis and metabolic reprogramming in glioma."],"pmcid":["PMC12417569"],"pubmed_authors":["Li G","Li X","Qian Z","Liu Z","He Y","Zhao Y","Song Z"],"additional_accession":[]},"is_claimable":false,"name":"NFIA-dependent upregulation of SMC4 promotes metastasis and metabolic reprogramming in glioma.","description":"<h4>Background</h4>Gliomas, particularly glioblastoma, are aggressive brain tumors with poor prognosis and unmet therapeutic needs. Structural maintenance of chromosomes 4 (SMC4), a core component of the condensin complex, is dysregulated in multiple cancers, but its role in glioma metabolism and metastasis remains unclear.<h4>Methods</h4>Using integrated multi-omics analyses of glioma datasets, we assessed SMC4 expression and its correlation with clinical outcomes. Functional studies in U-251MG and LN229 glioma cells including CCK-8, EdU, cell cycle, Transwell, and wound-healing assays were combined with subcutaneous xenograft and tail-vein metastasis mouse models to evaluate SMC4's effects on proliferation, migration, invasion, and metastasis. ECAR/OCR and rescue experiments validated SM","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025","modification":"2026-05-26T11:03:43.02Z","creation":"2026-05-24T03:07:30.636Z"},"accession":"S-EPMC12417569","cross_references":{"pubmed":["40933894"],"doi":["10.3389/fonc.2025.1624370"]}}