{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Ran R"],"funding":["Cancer Research UK","Breast Cancer Now","Wellcome Trust"],"pagination":["2624-2637"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7082223"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["39(12)"],"pubmed_abstract":["Epithelial to mesenchymal transition (EMT) is a dynamic process that drives cancer cell plasticity and is thought to play a major role in metastasis. Here we show, using MDA-MB-231 cells as a model, that the plasticity of at least some metastatic breast cancer cells is dependent on the transcriptional co-regulator CBFβ. We demonstrate that CBFβ is essential to maintain the mesenchymal phenotype of triple-negative breast cancer cells and that CBFβ-depleted cells undergo a mesenchymal to epithelial transition (MET) and re-organise into acini-like structures, reminiscent of those formed by epithelial breast cells. We subsequently show, using an inducible CBFβ system, that the MET can be reversed, thus demonstrating the plasticity of CBFβ-mediated EMT. Moreover, the MET can be reversed by expr"],"journal":["Oncogene"],"pubmed_title":["A role for CBFβ in maintaining the metastatic phenotype of breast cancer cells."],"pmcid":["PMC7082223"],"funding_grant_id":["C596/A17196","May2013","PhD Studentship","29799","S_1591"],"pubmed_authors":["Ran R","Shore P","Ottewell PD","Blyth K","Syamimi Ariffin N","Pegg HJ","Holen I","Harrison H","Ayub R","Deng W","Mason SM","Mastro A"],"additional_accession":[]},"is_claimable":false,"name":"A role for CBFβ in maintaining the metastatic phenotype of breast cancer cells.","description":"Epithelial to mesenchymal transition (EMT) is a dynamic process that drives cancer cell plasticity and is thought to play a major role in metastasis. Here we show, using MDA-MB-231 cells as a model, that the plasticity of at least some metastatic breast cancer cells is dependent on the transcriptional co-regulator CBFβ. We demonstrate that CBFβ is essential to maintain the mesenchymal phenotype of triple-negative breast cancer cells and that CBFβ-depleted cells undergo a mesenchymal to epithelial transition (MET) and re-organise into acini-like structures, reminiscent of those formed by epithelial breast cells. We subsequently show, using an inducible CBFβ system, that the MET can be reversed, thus demonstrating the plasticity of CBFβ-mediated EMT. Moreover, the MET can be reversed by expr","dates":{"release":"2020-01-01T00:00:00Z","publication":"2020 Mar","modification":"2025-05-29T20:05:38.487Z","creation":"2025-05-29T20:05:38.487Z"},"accession":"S-EPMC7082223","cross_references":{"pubmed":["32005976"],"doi":["10.1038/s41388-020-1170-2"]}}