ArticleScientific reports2019
SNAI1 recruits HDAC1 to suppress SNAI2 transcription during epithelial to mesenchymal transition.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 47 citations in OpenAlex.
- Comparative Transcriptomic Analysis of Oral Squamous Cell Carcinoma with Progressive Cisplatin Resistance.International journal of molecular sciences · 2026Article
- PBRM1-dependent PBAF targeting is required for EMT and metastasis in breast cancer.Science advances · 2026Article
- Decoding the Snail transcriptional network: its role in cancer progression and therapy.Biology direct · 2026Review
- Signalling pathways in hepatocellular carcinoma (HCC) metastasis and invasion: Molecular mechanisms and therapeutic implications.Biochemistry and biophysics reports · 2026Review
- Tigecycline suppresses colon cancer stem cells and impairs tumor engraftment by targeting SNAI1-regulated epithelial-mesenchymal transition.Acta pharmacologica Sinica · 2026Article
- A type of pancreatic cancer cells form cell clusters from a solitary condition in a primary ciliogenesis-dependent manner.Medical molecular morphology · 2025Article
- Construction and validation of a senescence-related gene signature for early prediction and treatment of osteoarthritis based on bioinformatics analysis.Scientific reports · 2024Article
- Regulating epithelial-mesenchymal plasticity from 3D genome organization.Communications biology · 2024Review
- The evolution of small molecule enzyme activators.RSC medicinal chemistry · 2023Review
- The Roles of Histone Deacetylases in the Regulation of Ovarian Cancer Metastasis.International journal of molecular sciences · 2023Review
- Article
- Role of epithelial-mesenchymal transition factor SNAI1 and its targets in ovarian cancer aggressiveness.Journal of cancer metastasis and treatment · 2023Article
- E-box binding transcription factors in cancer.Frontiers in oncology · 2023Review
- MAPKs in the early steps of senescence implemEMTation.Frontiers in cell and developmental biology · 2023Article
- Human Cytomegalovirus Induces Vitamin-D Resistance In Vitro by Dysregulating the Transcriptional Repressor Snail.Viruses · 2022Article
- PARP1-SNAI2 transcription axis drives resistance to PARP inhibitor, Talazoparib.Scientific reports · 2022Article
- 3D genome organization in the epithelial-mesenchymal transition spectrum.Genome biology · 2022Article
- Maternal soybean genistein on prevention of later-life breast cancer through inherited epigenetic regulations.Carcinogenesis · 2022Article
- Epithelial-mesenchymal transition and its transcription factors.Bioscience reports · 2022Review
- Chromatin accessibility and microRNA expression in nephron progenitor cells during kidney development.Genomics · 2022Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aberrant activation of epithelial to mesenchymal transition (EMT) associated factors were highly correlated with increased mortality in cancer patients. SNAIL family of transcriptional repressors comprised of three members, each of which were essentially associated with gastrulation and neural crest formation. Among which, SNAI1 and SNAI2 were efficiently induced during EMT and their expressions were correlated with poor clinical outcome in patients with breast, colon and ovarian carcinoma. In an ovarian cancer cell lines panel, we identified that SNAI1 and SNAI2 expressions were mutually exclusive, where SNAI1 predominantly represses SNAI2 expression. Detailed analysis of SNAI2 promoter region revealed that SNAI1 binds to two E-box sequences that mediated transcriptional repression. Through epigenetic inhibitor treatments, we identified that inhibition of histone deacetylase (HDAC) activity in SNAI1 overexpressing cells partially rescued SNAI2 expression. Importantly, we demonstrated a significant deacetylation of histone H3 and significant enrichments of HDAC1 and HDAC2 corepressors in both E-box regions of SNAI2 promoter. Our results suggested that SNAI1 repression on SNAI2 expression was predominantly mediated through the recruitment of the histone deacetylation machinery. Utilization of HDAC inhibitors would require additional profiling of SNAI1 activity and combined targeting of SNAI1 and HDACs might render efficient cancer treatment.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.