ArticleThe Journal of clinical investigation2012
Nkx3.1 and Myc crossregulate shared target genes in mouse and human prostate tumorigenesis.
Article in The Journal of clinical investigation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.
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Who cites it
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.
- Loss of the NKX3.1 tumorsuppressor promotes the TMPRSS2-ERG fusion gene expression in prostate cancer.BMC cancer · 2014Pooled it
- A functional variant in NKX3.1 associated with prostate cancer risk in the Selenium and Vitamin E Cancer Prevention Trial (SELECT).Cancer prevention research (Philadelphia, Pa.) · 2014Trial
- Exogenous testosterone exacerbates pre-neoplastic lesions in the prostate of NKX3.1-deficient mice.Laboratory animal research · 2026Article
- Mapping prostate cancer pathobiology: A review of genetically engineered mouse models (GEMMs).Gene · 2026Review
- QSOX1: A Mysterious Golgi-Localized Disulfide Bond Catalyst and an Emerging Cancer Regulator.Cancers · 2026Article
- Cellular heterogeneity and patterning strategies as revealed by upper respiratory epithelium single cell atlas.iScience · 2025Article
- Deletions ofBiomolecules · 2025Article
- Diverse landscape of genetically engineered mouse models: Genomic and molecular insights into prostate cancer.Cancer letters · 2024Review
- PIM Kinase Inhibitors as Novel Promising Therapeutic Scaffolds in Cancer Therapy.Current topics in medicinal chemistry · 2024Review
- In Vivo Models for Prostate Cancer Research.Cancers · 2022Review
- Targeting treatment options for castration-resistant prostate cancer.American journal of clinical and experimental urology · 2021Review
- Cellular and Molecular Mechanisms Underlying Prostate Cancer Development: Therapeutic Implications.Medicines (Basel, Switzerland) · 2019Review
- CHD1 Loss Alters AR Binding at Lineage-Specific Enhancers and Modulates Distinct Transcriptional Programs to Drive Prostate Tumorigenesis.Cancer cell · 2019Article
- Genetically Engineered Mouse Models of Prostate Cancer in the Postgenomic Era.Cold Spring Harbor perspectives in medicine · 2019Review
- The Homeodomain Transcription Factor NKX3.1 Modulates Bladder Outlet Obstruction Induced Fibrosis in Mice.Frontiers in pediatrics · 2019Article
- Transcriptional Regulation in Prostate Cancer.Cold Spring Harbor perspectives in medicine · 2018Review
- A blood biomarker for monitoring response to anti-EGFR therapy.Cancer biomarkers : section A of Disease markers · 2018Article
- Recent Advances in Liquid Biopsy in Patients With Castration Resistant Prostate Cancer.Frontiers in oncology · 2018Review
- Immunohistochemical panel to characterize canine prostate carcinomas according to aberrant p63 expression.PloS one · 2018Article
- PTEN loss and activation of K-RAS and β-catenin cooperate to accelerate prostate tumourigenesis.The Journal of pathology · 2017Article
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12 authors at 3 institutions in 1 country.
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Abstract
Cooperativity between oncogenic mutations is recognized as a fundamental feature of malignant transformation, and it may be mediated by synergistic regulation of the expression of pro- and antitumorigenic target genes. However, the mechanisms by which oncogenes and tumor suppressors coregulate downstream targets and pathways remain largely unknown. Here, we used ChIP coupled to massively parallel sequencing (ChIP-seq) and gene expression profiling in mouse prostates to identify direct targets of the tumor suppressor Nkx3.1. Further analysis indicated that a substantial fraction of Nkx3.1 target genes are also direct targets of the oncoprotein Myc. We also showed that Nkx3.1 and Myc bound to and crossregulated shared target genes in mouse and human prostate epithelial cells and that Nkx3.1 could oppose the transcriptional activity of Myc. Furthermore, loss of Nkx3.1 cooperated with concurrent overexpression of Myc to promote prostate cancer in transgenic mice. In human prostate cancer patients, dysregulation of shared NKX3.1/MYC target genes was associated with disease relapse. Our results indicate that NKX3.1 and MYC coregulate prostate tumorigenesis by converging on, and crossregulating, a common set of target genes. We propose that coregulation of target gene expression by oncogenic/tumor suppressor transcription factors may represent a general mechanism underlying the cooperativity of oncogenic mutations during tumorigenesis.
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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.