ArticleCancer research2014
Cell fate factor DACH1 represses YB-1-mediated oncogenic transcription and translation.
Article in Cancer research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
58 citing papers in PubMed, 81 citations in OpenAlex.
- NCBP1 stress signaling drives alternative S6K1 splicing inhibiting translation.Nature chemical biology · 2026Article
- Single-nucleus chromatin accessibility and transcriptomic map of breast tissues of women of diverse genetic ancestry.Nature medicine · 2024Article
- Autophagy Deficiency Induced by SAT1 Potentiates Tumor Progression in Triple-Negative Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Dach1 is essential for maintaining normal mature podocytes.PloS one · 2024Article
- S100A8/A9 as a risk factor for breast cancer negatively regulated by DACH1.Biomarker research · 2023Article
- Upregulated PARP1 confers breast cancer resistance to CDK4/6 inhibitors via YB-1 phosphorylation.Experimental hematology & oncology · 2023Article
- Article
- Exploiting E3 ubiquitin ligases to reeducate the tumor microenvironment for cancer therapy.Experimental hematology & oncology · 2023Review
- Retinal determination gene networks: from biological functions to therapeutic strategies.Biomarker research · 2023Review
- The DACH1 gene is frequently deleted in prostate cancer, restrains prostatic intraepithelial neoplasia, decreases DNA damage repair, and predicts therapy responses.Research square · 2023Article
- Genetic variants in RNA mCancer medicine · 2023Article
- YB-1 is a positive regulator of KLF5 transcription factor in basal-like breast cancer.Cell death and differentiation · 2022Article
- SIX1 Predicts Poor Prognosis and Facilitates the Progression of Non-small Lung Cancer via Activating the Notch Signaling Pathway.Journal of Cancer · 2022Article
- YB-1 Phosphorylation at Serine 209 Inhibits Its Nuclear Translocation.International journal of molecular sciences · 2021Article
- Sequence-specific recognition of a coding segment of humanRSC advances · 2021Article
- DACH1 inhibits breast cancer cell invasion and metastasis by down-regulating the transcription of matrix metalloproteinase 9.Cell death discovery · 2021Article
- A comprehensive review of the functions of YB-1 in cancer stemness, metastasis and drug resistance.Cellular signalling · 2021Review
- Y box binding protein 1 inhibition as a targeted therapy for ovarian cancer.Cell chemical biology · 2021Article
- Mechanisms Governing Metabolic Heterogeneity in Breast Cancer and Other Tumors.Frontiers in oncology · 2021Review
- Article
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 2 countries.
Funding
Abstract
The epithelial-mesenchymal transition (EMT) enhances cellular invasiveness and confers tumor cells with cancer stem cell-like characteristics, through transcriptional and translational mechanisms. The mechanisms maintaining transcriptional and translational repression of EMT and cellular invasion are poorly understood. Herein, the cell fate determination factor Dachshund (DACH1), suppressed EMT via repression of cytoplasmic translational induction of Snail by inactivating the Y box-binding protein (YB-1). In the nucleus, DACH1 antagonized YB-1-mediated oncogenic transcriptional modules governing cell invasion. DACH1 blocked YB-1-induced mammary tumor growth and EMT in mice. In basal-like breast cancer, the reduced expression of DACH1 and increased YB-1 correlated with poor metastasis-free survival. The loss of DACH1 suppression of both cytoplasmic translational and nuclear transcriptional events governing EMT and tumor invasion may contribute to poor prognosis in basal-like forms of breast cancer, a relatively aggressive disease subtype.
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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.