ArticleCancer research2009
The cell fate determination factor DACH1 is expressed in estrogen receptor-alpha-positive breast cancer and represses estrogen receptor-alpha signaling.
Article in Cancer research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 60 citations in OpenAlex.
- Lung-derived soluble factors support stemness/plasticity and metastatic behaviour of breast cancer cells via the FGF2-DACH1 axis.Clinical & experimental metastasis · 2024Article
- Dach1 is essential for maintaining normal mature podocytes.PloS one · 2024Article
- Estrogen Receptor Signaling in Breast Cancer.Cancers · 2023Review
- Retinal determination gene networks: from biological functions to therapeutic strategies.Biomarker research · 2023Review
- Progestin Resistance and Corresponding Management of Abnormal Endometrial Hyperplasia and Endometrial Carcinoma.Cancers · 2022Review
- YB-1 is a positive regulator of KLF5 transcription factor in basal-like breast cancer.Cell death and differentiation · 2022Article
- The Function of circRNA-0047604 in Regulating the Tumor Suppressor Gene DACH1 in Breast Cancer.BioMed research international · 2022Article
- Sequence-specific recognition of a coding segment of humanRSC advances · 2021Article
- Forkhead box M1 over-expression and dachshund homolog 1 down-regulation as novel biomarkers for progression of endometrial carcinoma in Egyptian patients.Contemporary oncology (Poznan, Poland) · 2021Article
- MicroRNA-362 negatively and positively regulates SMAD4 expression in TGF-β/SMAD signaling to suppress cell migration and invasion.International journal of medical sciences · 2021Article
- RDGN-based predictive model for the prognosis of breast cancer.Experimental hematology & oncology · 2020Article
- DACH1 mutation frequency in endometrial cancer is associated with high tumor mutation burden.PloS one · 2020Article
- Estrogen receptor coregulator binding modulator (ERX-11) enhances the activity of CDK4/6 inhibitors against estrogen receptor-positive breast cancers.Breast cancer research : BCR · 2019Article
- DACH1 suppresses epithelial to mesenchymal transition (EMT) through Notch1 pathway and reverses progestin resistance in endometrial carcinoma.Cancer medicine · 2019Article
- Dachshund Depletion Disrupts Mammary Gland Development and Diverts the Composition of the Mammary Gland Progenitor Pool.Stem cell reports · 2019Article
- PELP1 Suppression Inhibits Gastric Cancer Through Downregulation of c-Src-PI3K-ERK Pathway.Frontiers in oncology · 2019Article
- Effect of DACH1 on proliferation and invasion of laryngeal squamous cell carcinoma.Head & face medicine · 2018Article
- DACH1 antagonizes CXCL8 to repress tumorigenesis of lung adenocarcinoma and improve prognosis.Journal of hematology & oncology · 2018Article
- The regulation of cytokine signaling by retinal determination gene network pathway in cancer.OncoTargets and therapy · 2018Review
- DACH1 inhibits glioma invasion and tumor growth via the Wnt/catenin pathway.OncoTargets and therapy · 2018Article
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 1 country.
Funding
Abstract
The Dachshund (dac) gene, initially cloned as a dominant inhibitor of the Drosophila hyperactive EGFR mutant ellipse, encodes a key component of the cell fate determination pathway involved in Drosophila eye development. Analysis of more than 2,200 breast cancer samples showed improved survival by some 40 months in patients whose tumors expressed DACH1. Herein, DACH1 and estrogen receptor-alpha (ERalpha) expressions were inversely correlated in human breast cancer. DACH1 bound and inhibited ERalpha function. Nuclear DACH1 expression inhibited estradiol (E(2))-induced DNA synthesis and cellular proliferation. DACH1 bound ERalpha in immunoprecipitation-Western blotting, associated with ERalpha in chromatin immunoprecipitation, and inhibited ERalpha transcriptional activity, requiring a conserved DS domain. Proteomic analysis identified proline, glutamic acid, and leucine rich protein 1 (PELP1) as a DACH1-binding protein. The DACH1 COOH terminus was required for binding to PELP1. DACH1 inhibited induction of ERalpha signaling. E(2) recruited ERalpha and disengaged corepressors from DACH1 at an endogenous ER response element, allowing PELP1 to serve as an ERalpha coactivator. DACH1 expression, which is lost in poor prognosis human breast cancer, functions as an endogenous inhibitor of ERalpha function.
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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.