{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["240(11)"],"submitter":["Chen CY"],"funding":["This study was supported by the National Science and Technology Council in Taiwan (to WWC, grant numbers 110-2320-B-040-026, 111-2320-B-040-007-MY3, and 114-2320-B-040-005-MY3) and Tungs' Taichung MetroHarbor Hospital (to CYC, grant number TTMHH-R1140032)."],"pubmed_abstract":["Endometrial cancer (EC) is the most prevalent gynecological malignancy globally. Here, we explored the role of E74-like ETS transcription factor 4 (ELF4) in EC progression. Using the TISIDB web tool to analyze TCGA data, we found that elevated ELF4 expression correlates with higher histological grades and reduced overall survival in EC patients. Tissue microarray analysis confirmed a grade-dependent increase in ELF4 protein levels. Knockdown of ELF4 in EC cell lines (AN3CA, HEC-1A) and patient-derived EC cells suppressed proliferation, cell cycle progression, and cancer stem cell (CSC) activity. Database analysis and RNA interference identified cyclin-dependent kinase 6 (CDK6) as a downstream target of ELF4. ELF4 silencing reduced CDK6 mRNA and protein expression, while chromatin immunopre"],"journal":["Journal of cellular physiology"],"pagination":["e70113"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12645360"],"repository":["biostudies-literature"],"pubmed_title":["ELF4/TRIB3/CDK6 Axis Promotes Cancer Stem Cell Activity in Endometrial Cancer."],"pmcid":["PMC12645360"],"pubmed_authors":["Lee YC","Chang WW","Chen CY","Huang YH","Wang WL"],"additional_accession":[]},"is_claimable":false,"name":"ELF4/TRIB3/CDK6 Axis Promotes Cancer Stem Cell Activity in Endometrial Cancer.","description":"Endometrial cancer (EC) is the most prevalent gynecological malignancy globally. Here, we explored the role of E74-like ETS transcription factor 4 (ELF4) in EC progression. Using the TISIDB web tool to analyze TCGA data, we found that elevated ELF4 expression correlates with higher histological grades and reduced overall survival in EC patients. Tissue microarray analysis confirmed a grade-dependent increase in ELF4 protein levels. Knockdown of ELF4 in EC cell lines (AN3CA, HEC-1A) and patient-derived EC cells suppressed proliferation, cell cycle progression, and cancer stem cell (CSC) activity. Database analysis and RNA interference identified cyclin-dependent kinase 6 (CDK6) as a downstream target of ELF4. ELF4 silencing reduced CDK6 mRNA and protein expression, while chromatin immunopre","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Nov","modification":"2026-06-05T18:53:54.485Z","creation":"2026-05-20T03:14:26.358Z"},"accession":"S-EPMC12645360","cross_references":{"pubmed":["41287970"],"doi":["10.1002/jcp.70113"]}}