ArticleNucleic acids research2017
Interaction with ZMYND11 mediates opposing roles of Ras-responsive transcription factors ETS1 and ETS2.
Article in Nucleic acids research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 23 citations in OpenAlex.
- Decoding ZMYND11-Related Syndromic Intellectual Disability: From Epigenetic Mysteries to Therapeutic Horizons.Neuroscience bulletin · 2026Article
- Multiple ETS family transcription factors bind mutant p53 via distinct interaction regions.FEBS letters · 2026Article
- Novel intermolecular zinc fingers and redox-driven conformational changes dictate tumor suppressor ZMYND11's role in cooperative recognition of diverse targets.Nucleic acids research · 2026Article
- MiR-19b-3p facilitates colorectal cancer metastasis by mediating the crosstalk between tumor-associated endothelial cells and malignant cells.Frontiers in oncology · 2026Article
- ZMYND11 functions in bimodal regulation of latent genes and brain-like splicing to safeguard corticogenesis.Nature communications · 2025Article
- ETS-1 in tumor immunology: implications for novel anti-cancer strategies.Frontiers in immunology · 2025Review
- ETS2 targets ZMYND11 to inhibit thyroid cancer progression via the mTOR signaling pathway.PloS one · 2025Article
- DKK1+ tumor cells inhibited the infiltration of CCL19+ fibroblasts and plasma cells contributing to worse immunotherapy response in hepatocellular carcinoma.Cell death & disease · 2024Article
- Machine learning-based biomarker screening for acute myeloid leukemia prognosis and therapy from diverse cell-death patterns.Scientific reports · 2024Article
- Identification of genetic associations between acute myocardial infarction and non-small cell lung cancer.Frontiers in molecular biosciences · 2024Article
- Epigenome-wide development and validation of a prognostic methylation score in intrahepatic cholangiocarcinoma based on machine learning strategies.Hepatobiliary surgery and nutrition · 2023Article
- Distinct Prognostic and Immunological Roles of ETS1 and ETS2: A Pan-Cancer Analysis.BioMed research international · 2023Article
- TLR13 contributes to skeletal muscle atrophy by increasing insulin resistance in chronic kidney disease.Cell proliferation · 2022Article
- Survival Risk Prediction Models of Gliomas Based on IDH and 1p/19q.Journal of Cancer · 2020Article
- Article
- Molecular dissection of the oncogenic role of ETS1 in the mesenchymal subtypes of head and neck squamous cell carcinoma.PLoS genetics · 2019Article
- EGF suppresses the expression of miR-124a in pancreatic β cell lines via ETS2 activation through the MEK and PI3K signaling pathways.International journal of biological sciences · 2019Article
- The Transcriptional Repressor BS69 is a Conserved Target of the E1A Proteins from Several Human Adenovirus Species.Viruses · 2018Article
- Article
- Common ELF1 deletion in prostate cancer bolsters oncogenic ETS function, inhibits senescence and promotes docetaxel resistance.Genes & cancer · 2018Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aberrant activation of RAS/MAPK signaling is a driver of over one third of all human carcinomas. The homologous transcription factors ETS1 and ETS2 mediate activation of gene expression programs downstream of RAS/MAPK signaling. ETS1 is important for oncogenesis in many tumor types. However, ETS2 can act as an oncogene in some cellular backgrounds, and as a tumor suppressor in others, and the molecular mechanism responsible for this cell-type specific function remains unknown. Here, we show that ETS1 and ETS2 can regulate a cell migration gene expression program in opposite directions, and provide the first comparison of the ETS1 and ETS2 cistromes. This genomic data and an ETS1 deletion line reveal that the opposite function of ETS2 is a result of binding site competition and transcriptional attenuation due to weaker transcriptional activation by ETS2 compared to ETS1. This weaker activation was mapped to the ETS2 N-terminus and a specific interaction with the co-repressor ZMYND11 (BS69). Furthermore, ZMYND11 expression levels in patient tumors correlated with oncogenic versus tumor suppressive roles of ETS2. Therefore, these data indicate a novel and specific mechanism allowing ETS2 to switch between oncogenic and tumor suppressive functions in a cell-type specific manner.
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Registered trials
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