{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Liang H"],"funding":["Breast Cancer Research Foundation (BCRF)","Breast Cancer Research Foundation","U.S. Department of Health &amp; Human Services | NIH | National Cancer Institute","NCI NIH HHS"],"pagination":["986-1002"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12480652"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["133(7)"],"pubmed_abstract":["<h4>Background</h4>The hybrid EMT state is a key driver of tumour regenerative and metastatic potential; however, the mechanism whereby this programme regulates tumour stemness with respect to self-renewal and differentiation remains unclear.<h4>Methods</h4>We isolated epithelial/mesenchymal (E/M) (CD104<sup>high</sup>CD44<sup>high</sup>) and mesenchymal (M) (CD104<sup>low</sup> CD44<sup>high</sup>) subpopulations from basal-like breast cancer cell lines. These were assayed for tumour-initiating potential and organoid-forming ability, as well as for transcriptional regulators of the hybrid EMT state by RNA and ATAC-sequencing, and their regulation by the Wnt/ERK/CDK4/6 signalling pathway.<h4>Results</h4>E/M cells were endowed with organoid-forming ability as well as by tumour-initiating an"],"journal":["British journal of cancer"],"pubmed_title":["Wnt/ERK/CDK4/6 activation in the partial EMT state coordinates mammary cancer stemness with self-renewal and inhibition of differentiation."],"pmcid":["PMC12480652"],"funding_grant_id":["P01 CA257885","BCRF-18-066"],"pubmed_authors":["Norton L","Kumar V","Griffen A","Zhang J","Ren Z","Sivalingam K","LaFave LM","Hazan RB","Wang J","Benard O","Liang H","Zhang X","Suyama K","de Simone Benito E"],"additional_accession":[]},"is_claimable":false,"name":"Wnt/ERK/CDK4/6 activation in the partial EMT state coordinates mammary cancer stemness with self-renewal and inhibition of differentiation.","description":"<h4>Background</h4>The hybrid EMT state is a key driver of tumour regenerative and metastatic potential; however, the mechanism whereby this programme regulates tumour stemness with respect to self-renewal and differentiation remains unclear.<h4>Methods</h4>We isolated epithelial/mesenchymal (E/M) (CD104<sup>high</sup>CD44<sup>high</sup>) and mesenchymal (M) (CD104<sup>low</sup> CD44<sup>high</sup>) subpopulations from basal-like breast cancer cell lines. These were assayed for tumour-initiating potential and organoid-forming ability, as well as for transcriptional regulators of the hybrid EMT state by RNA and ATAC-sequencing, and their regulation by the Wnt/ERK/CDK4/6 signalling pathway.<h4>Results</h4>E/M cells were endowed with organoid-forming ability as well as by tumour-initiating an","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Oct","modification":"2026-06-03T23:33:23.498Z","creation":"2026-05-03T03:11:27.453Z"},"accession":"S-EPMC12480652","cross_references":{"pubmed":["40764669"],"doi":["10.1038/s41416-025-03074-6"]}}