{"entity": "publication", "iuid": "d0929650e1a94e0a900ebd641c5a056f", "timestamp": "2026-04-20T03:39:11.994Z", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/d0929650e1a94e0a900ebd641c5a056f.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/d0929650e1a94e0a900ebd641c5a056f"}}, "title": "Genomewide binding of transcription factor Snail1 in triple-negative breast cancer cells.", "authors": [{"family": "Maturi", "given": "Varun", "initials": "V"}, {"family": "Mor\u00e9n", "given": "Anita", "initials": "A"}, {"family": "Enroth", "given": "Stefan", "initials": "S"}, {"family": "Heldin", "given": "Carl-Henrik", "initials": "CH"}, {"family": "Moustakas", "given": "Aristidis", "initials": "A"}], "type": "journal article", "published": "2018-06-00", "journal": {"title": "Mol Oncol", "issn": "1878-0261", "volume": "12", "issue": "7", "pages": "1153-1174", "issn-l": "1574-7891"}, "abstract": "Transcriptional regulation mediated by the zinc finger protein Snail1 controls early embryogenesis. By binding to the epithelial tumor suppressor CDH1 gene, Snail1 initiates the epithelial-mesenchymal transition (EMT). The EMT generates stem-like cells and promotes invasiveness during cancer progression. Accordingly, Snail1 mRNA and protein is abundantly expressed in triple-negative breast cancers with enhanced metastatic potential and phenotypic signs of the EMT. Such high endogenous Snail1 protein levels permit quantitative chromatin immunoprecipitation-sequencing (ChIP-seq) analysis. Snail1 associated with 185 genes at cis regulatory regions in the Hs578T triple-negative breast cancer cell model. These genes include morphogenetic regulators and signaling components that control polarized differentiation. Using the CRISPR/Cas9 system in Hs578T cells, a double deletion of 10\u00a0bp each was engineered into the first exon and into the second exon-intron junction of Snail1, suppressing Snail1 expression and causing misregulation of several hundred genes. Specific attention to regulators of chromatin organization provides a possible link to new phenotypes uncovered by the Snail1 loss-of-function mutation. On the other hand, genetic inactivation of Snail1 was not sufficient to establish a full epithelial transition to these tumor cells. Thus, Snail1 contributes to the malignant phenotype of breast cancer cells via diverse new mechanisms.", "doi": "10.1002/1878-0261.12317", "pmid": "29729076", "labels": {"Affiliated researcher": null}, "xrefs": [{"db": "pmc", "key": "PMC6026864"}], "notes": [], "created": "2019-01-17T13:52:20.885Z", "modified": "2019-01-17T13:52:20.904Z"}