<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Ran R</submitter><funding>Cancer Research UK</funding><funding>Breast Cancer Now</funding><funding>Wellcome Trust</funding><pagination>2624-2637</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7082223</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>39(12)</volume><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</pubmed_abstract><journal>Oncogene</journal><pubmed_title>A role for CBFβ in maintaining the metastatic phenotype of breast cancer cells.</pubmed_title><pmcid>PMC7082223</pmcid><funding_grant_id>C596/A17196</funding_grant_id><funding_grant_id>May2013</funding_grant_id><funding_grant_id>PhD Studentship</funding_grant_id><funding_grant_id>29799</funding_grant_id><funding_grant_id>S_1591</funding_grant_id><pubmed_authors>Ran R</pubmed_authors><pubmed_authors>Shore P</pubmed_authors><pubmed_authors>Ottewell PD</pubmed_authors><pubmed_authors>Blyth K</pubmed_authors><pubmed_authors>Syamimi Ariffin N</pubmed_authors><pubmed_authors>Pegg HJ</pubmed_authors><pubmed_authors>Holen I</pubmed_authors><pubmed_authors>Harrison H</pubmed_authors><pubmed_authors>Ayub R</pubmed_authors><pubmed_authors>Deng W</pubmed_authors><pubmed_authors>Mason SM</pubmed_authors><pubmed_authors>Mastro A</pubmed_authors></additional><is_claimable>false</is_claimable><name>A role for CBFβ in maintaining the metastatic phenotype of breast cancer cells.</name><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</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020 Mar</publication><modification>2025-05-29T20:05:38.487Z</modification><creation>2025-05-29T20:05:38.487Z</creation></dates><accession>S-EPMC7082223</accession><cross_references><pubmed>32005976</pubmed><doi>10.1038/s41388-020-1170-2</doi></cross_references></HashMap>