ArticleCancer research2013
EYA1 phosphatase function is essential to drive breast cancer cell proliferation through cyclin D1.
Article in Cancer research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed, 93 citations in OpenAlex.
- A single-cell atlas revealing cellular heterogeneity across healthy and diseased human thymus.Nature communications · 2026Article
- EYA1 promotes tumor angiogenesis in colorectal cancer by activating HIF-1β through LSD2-mediated H3K4me2 demethylation.Journal of cancer research and clinical oncology · 2025Article
- SENP5 drives breast cancer progression through deSUMOYlation of CDK1.Breast cancer research : BCR · 2025Article
- EYA3 regulation of NF-κB and CCL2 suppresses cytotoxic NK cells in the premetastatic niche to promote TNBC metastasis.Science advances · 2025Article
- The Ku70-SIX1-GPT2 axis regulates alpha-ketoglutarate metabolism to drive progression of prostate cancer.Oncogene · 2025Article
- SENP3 mediates deSUMOylation of SIX1 to promote prostate cancer proliferation and migration.Cellular & molecular biology letters · 2024Article
- Implications of ITCH-mediated ubiquitination of SIX1 on CDC27-cyclinB1 signaling in nasopharyngeal carcinoma.Scientific reports · 2024Article
- All eyes on Eya: A unique transcriptional co-activator and phosphatase in cancer.Biochimica et biophysica acta. Reviews on cancer · 2024Review
- The Eyes Absent family members EYA4 and EYA1 promote PLK1 activation and successful mitosis through tyrosine dephosphorylation.Nature communications · 2024Article
- In Vitro Phosphatase Assays for the Eya2 Tyrosine Phosphatase.Methods in molecular biology (Clifton, N.J.) · 2024Article
- EYA2 tyrosine phosphatase inhibition reduces MYC and prevents medulloblastoma progression.Neuro-oncology · 2023Article
- Dephosphorylation of Six2Y129 protects tyrosine hydroxylase-positive cells in SNpc by regulating TEA domain 1 expression.iScience · 2023Article
- The value of EYA1/3/4 in clear cell renal cell carcinoma: a study from multiple databases.Scientific reports · 2023Article
- Retinal determination gene networks: from biological functions to therapeutic strategies.Biomarker research · 2023Review
- The transcriptional coactivator Eya1 exerts transcriptional repressive activity by interacting with REST corepressors and REST-binding sequences to maintain nephron progenitor identity.Nucleic acids research · 2022Article
- A SIX1 degradation inducer blocks excessive proliferation of prostate cancer.International journal of biological sciences · 2022Article
- Targeting EYA2 tyrosine phosphatase activity in glioblastoma stem cells induces mitotic catastrophe.The Journal of experimental medicine · 2021Article
- Phage display targeting identifies EYA1 as a regulator of glioblastoma stem cell maintenance and proliferation.Stem cells (Dayton, Ohio) · 2021Article
- A novel method to identify gene interaction patterns.BMC genomics · 2021Article
- A new role of GRP75-USP1-SIX1 protein complex in driving prostate cancer progression and castration resistance.Oncogene · 2021Article
4 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
The Drosophila Eyes Absent Homologue 1 (EYA1) is a component of the retinal determination gene network and serves as an H2AX phosphatase. The cyclin D1 gene encodes the regulatory subunits of a holoenzyme that phosphorylates and inactivates the pRb protein. Herein, comparison with normal breast showed that EYA1 is overexpressed with cyclin D1 in luminal B breast cancer subtype. EYA1 enhanced breast tumor growth in mice in vivo, requiring the phosphatase domain. EYA1 enhanced cellular proliferation, inhibited apoptosis, and induced contact-independent growth and cyclin D1 abundance. The induction of cellular proliferation and cyclin D1 abundance, but not apoptosis, was dependent upon the EYA1 phosphatase domain. The EYA1-mediated transcriptional induction of cyclin D1 occurred via the AP-1-binding site at -953 and required the EYA1 phosphatase function. The AP-1 mutation did not affect SIX1-dependent activation of cyclin D1. EYA1 was recruited in the context of local chromatin to the cyclin D1 AP-1 site. The EYA1 phosphatase function determined the recruitment of CBP, RNA polymerase II, and acetylation of H3K9 at the cyclin D1 gene AP-1 site regulatory region in the context of local chromatin. The EYA1 phosphatase regulates cell-cycle control via transcriptional complex formation at the cyclin D1 promoter.
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Registered trials
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.