{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zhang J"],"funding":["MOH | National Medical Research Council","Agency for Science, Technology and Research","National Research Foundation Singapore"],"pagination":["2439"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10147683"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["14(1)"],"pubmed_abstract":["Cancer cells undergo transcriptional reprogramming to drive tumor progression and metastasis. Using cancer cell lines and patient-derived tumor organoids, we demonstrate that loss of the negative elongation factor (NELF) complex inhibits breast cancer development through downregulating epithelial-mesenchymal transition (EMT) and stemness-associated genes. Quantitative multiplexed Rapid Immunoprecipitation Mass spectrometry of Endogenous proteins (qPLEX-RIME) further reveals a significant rewiring of NELF-E-associated chromatin partners as a function of EMT and a co-option of NELF-E with the key EMT transcription factor SLUG. Accordingly, loss of NELF-E leads to impaired SLUG binding on chromatin. Through integrative transcriptomic and genomic analyses, we identify the histone acetyltransfe"],"journal":["Nature communications"],"pubmed_title":["Dependency of NELF-E-SLUG-KAT2B epigenetic axis in breast cancer carcinogenesis."],"pmcid":["PMC10147683"],"funding_grant_id":["UIBR","NRF-CRP26-2021-0001","NMRC-OFIRG21nov-0027","NRF-NRFF2016-06","NMRC-OFIRG21jun-0101"],"pubmed_authors":["Chen BJ","Zhang J","Hu Z","Yeo CJ","Sobota RM","Raju A","Sou IF","Lakshmanan M","Tan EY","Tam WL","Tee WW","Leong HF","Kang J","Lim YT","Rajarethinam R","Tan DEK","Pathak E","Vaiyapuri TS","Chung HH","Lau KW","McClurg UL","Tergaonkar V","Tian Y","Wong ESM","Ser Z","Tan SYX"],"additional_accession":[]},"is_claimable":false,"name":"Dependency of NELF-E-SLUG-KAT2B epigenetic axis in breast cancer carcinogenesis.","description":"Cancer cells undergo transcriptional reprogramming to drive tumor progression and metastasis. Using cancer cell lines and patient-derived tumor organoids, we demonstrate that loss of the negative elongation factor (NELF) complex inhibits breast cancer development through downregulating epithelial-mesenchymal transition (EMT) and stemness-associated genes. Quantitative multiplexed Rapid Immunoprecipitation Mass spectrometry of Endogenous proteins (qPLEX-RIME) further reveals a significant rewiring of NELF-E-associated chromatin partners as a function of EMT and a co-option of NELF-E with the key EMT transcription factor SLUG. Accordingly, loss of NELF-E leads to impaired SLUG binding on chromatin. Through integrative transcriptomic and genomic analyses, we identify the histone acetyltransfe","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Apr","modification":"2026-05-28T11:56:38.213Z","creation":"2025-02-19T02:26:23.259Z"},"accession":"S-EPMC10147683","cross_references":{"pubmed":["37117180"],"doi":["10.1038/s41467-023-38132-1"]}}