ArticleMolecular oncology2018
Genomewide binding of transcription factor Snail1 in triple-negative breast cancer cells.
Article in Molecular oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 31 citations in OpenAlex.
- SNAI1 ablation alters integrin-mediated adhesion and endocytic fate.Cell death & disease · 2026Article
- Gut microbiota-regulated tryptophan metabolism in breast cancer: mechanisms and therapeutic perspectives.Frontiers in oncology · 2026Review
- Inhibitory Impact of the Amino Benzoic Derivative DAB-2-28 on the Process of Epithelial-Mesenchymal Transition in Human Breast Cancer Cells.Molecules (Basel, Switzerland) · 2025Article
- TFAP2A downregulation mediates tumor-suppressive effect of miR-8072 in triple-negative breast cancer via inhibiting SNAI1 transcription.Breast cancer research : BCR · 2024Article
- Mitotic kinases are emerging therapeutic targets against metastatic breast cancer.Cell division · 2024Review
- All eyes on Eya: A unique transcriptional co-activator and phosphatase in cancer.Biochimica et biophysica acta. Reviews on cancer · 2024Review
- Review
- Nanomaterial-assisted CRISPR gene-engineering - A hallmark for triple-negative breast cancer therapeutics advancement.Materials today. Bio · 2022Review
- Loss of SNAI1 induces cellular plasticity in invasive triple-negative breast cancer cells.Cell death & disease · 2022Article
- Triptonide effectively inhibits triple-negative breast cancer metastasis through concurrent degradation of Twist1 and Notch1 oncoproteins.Breast cancer research : BCR · 2021Article
- Liprins in oncogenic signaling and cancer cell adhesion.Oncogene · 2021Review
- TGFβ promotes widespread enhancer chromatin opening and operates on genomic regulatory domains.Nature communications · 2020Article
- Article
- The Impact of CRISPR-Cas9 on Age-related Disorders: From Pathology to Therapy.Aging and disease · 2020Review
- EMT signaling: potential contribution of CRISPR/Cas gene editing.Cellular and molecular life sciences : CMLS · 2020Review
- Expression and clinical significance of WWOX, Elf5, Snail1 and EMT related factors in epithelial ovarian cancer.Oncology letters · 2020Article
- MicroRNA-138-5p targets the NFIB-Snail1 axis to inhibit colorectal cancer cell migration and chemoresistance.Cancer cell international · 2020Article
- G9a and histone deacetylases are crucial for Snail2-mediated E-cadherin repression and metastasis in hepatocellular carcinoma.Cancer science · 2019Article
- Article
- Uronic acid pathway metabolites regulate mesenchymal transition and invasiveness in lung adenocarcinoma.Biotarget · 2019Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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 bp 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.
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