ArticleThe Journal of biological chemistry2011
Cell fate determination factor Dachshund reprograms breast cancer stem cell function.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 92 citations in OpenAlex.
- PPARγ acetylation governs mammary adenocarcinoma tumor growth via acetylated residues that determine DNA sequence-specific binding.Oncogene · 2025Article
- Lung-derived soluble factors support stemness/plasticity and metastatic behaviour of breast cancer cells via the FGF2-DACH1 axis.Clinical & experimental metastasis · 2024Article
- S100A8/A9 as a risk factor for breast cancer negatively regulated by DACH1.Biomarker research · 2023Article
- Estrogen Receptor Signaling in Breast Cancer.Cancers · 2023Review
- Retinal determination gene networks: from biological functions to therapeutic strategies.Biomarker research · 2023Review
- Antibiofilm and anticancer activities of unripe and ripe Azadirachta indica (neem) seed extracts.BMC complementary medicine and therapies · 2022Article
- Dach1 transcription factor regulates the expression of peripheral node addressin and lymphocyte trafficking in lymph nodes.Current research in immunology · 2022Article
- The Function of circRNA-0047604 in Regulating the Tumor Suppressor Gene DACH1 in Breast Cancer.BioMed research international · 2022Article
- Reporter gene systems for the identification and characterization of cancer stem cells.World journal of stem cells · 2021Review
- Novel mechanistic targets of forkhead box Q1 transcription factor in human breast cancer cells.Molecular carcinogenesis · 2020Article
- Inhibitory Effects of Tangeretin, A Citrus Peel-Derived Flavonoid, on Breast Cancer Stem Cell Formation through Suppression of Stat3 Signaling.Molecules (Basel, Switzerland) · 2020Article
- RDGN-based predictive model for the prognosis of breast cancer.Experimental hematology & oncology · 2020Article
- Pranlukast Antagonizes CD49f and Reduces Stemness in Triple-Negative Breast Cancer Cells.Drug design, development and therapy · 2020Article
- Human eye conditions: insights from the fly eye.Human genetics · 2019Review
- Dachshund Depletion Disrupts Mammary Gland Development and Diverts the Composition of the Mammary Gland Progenitor Pool.Stem cell reports · 2019Article
- CXCL1 as an Unfavorable Prognosis Factor Negatively Regulated by DACH1 in Non-small Cell Lung Cancer.Frontiers in oncology · 2019Article
- Effect of DACH1 on proliferation and invasion of laryngeal squamous cell carcinoma.Head & face medicine · 2018Article
- Transcription factor profiling identifies Sox9 as regulator of proliferation and differentiation in corneal epithelial stem/progenitor cells.Scientific reports · 2018Article
- DACH1 antagonizes CXCL8 to repress tumorigenesis of lung adenocarcinoma and improve prognosis.Journal of hematology & oncology · 2018Article
- 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
14 authors at 5 institutions in 2 countries.
Funding
Abstract
The cell fate determination factor Dachshund was cloned as a dominant inhibitor of the hyperactive epidermal growth factor receptor ellipse. The expression of Dachshund is lost in human breast cancer associated with poor prognosis. Breast tumor-initiating cells (TIC) may contribute to tumor progression and therapy resistance. Here, endogenous DACH1 was reduced in breast cancer cell lines with high expression of TIC markers and in patient samples of the basal breast cancer phenotype. Re-expression of DACH1 reduced new tumor formation in serial transplantations in vivo, reduced mammosphere formation, and reduced the proportion of CD44(high)/CD24(low) breast tumor cells. Conversely, lentiviral shRNA to DACH1 increased the breast (B)TIC population. Genome-wide expression studies of mammary tumors demonstrated DACH1 repressed a molecular signature associated with stem cells (SOX2, Nanog, and KLF4) and genome-wide ChIP-seq analysis identified DACH1 binding to the promoter of the Nanog, KLF4, and Lin28 genes. KLF4/c-Myc and Oct4/Sox2 antagonized DACH1 repression of BTIC. Mechanistic studies demonstrated DACH1 directly repressed the Nanog and Sox2 promoters via a conserved domain. Endogenous DACH1 regulates BTIC in vitro and in vivo.
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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.