<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>15</volume><submitter>Li G</submitter><pubmed_abstract>&lt;h4>Background&lt;/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.&lt;h4>Methods&lt;/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</pubmed_abstract><journal>Frontiers in oncology</journal><pagination>1624370</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12417569</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>NFIA-dependent upregulation of SMC4 promotes metastasis and metabolic reprogramming in glioma.</pubmed_title><pmcid>PMC12417569</pmcid><pubmed_authors>Li G</pubmed_authors><pubmed_authors>Li X</pubmed_authors><pubmed_authors>Qian Z</pubmed_authors><pubmed_authors>Liu Z</pubmed_authors><pubmed_authors>He Y</pubmed_authors><pubmed_authors>Zhao Y</pubmed_authors><pubmed_authors>Song Z</pubmed_authors></additional><is_claimable>false</is_claimable><name>NFIA-dependent upregulation of SMC4 promotes metastasis and metabolic reprogramming in glioma.</name><description>&lt;h4>Background&lt;/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.&lt;h4>Methods&lt;/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</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025</publication><modification>2026-05-26T11:03:43.02Z</modification><creation>2026-05-24T03:07:30.636Z</creation></dates><accession>S-EPMC12417569</accession><cross_references><pubmed>40933894</pubmed><doi>10.3389/fonc.2025.1624370</doi></cross_references></HashMap>