ArticleBritish journal of cancer2014
Hypoxia triggers a Nur77-β-catenin feed-forward loop to promote the invasive growth of colon cancer cells.
Article in British journal of cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 48 citations in OpenAlex.
- Controversy and multiple roles of the solitary nucleus receptor Nur77 in disease and physiology.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Review
- Nur77 protects the bladder urothelium from intracellular bacterial infection.Nature communications · 2024Article
- Delineating the role of nuclear receptors in colorectal cancer, a focused review.Discover oncology · 2024Review
- The role of hypoxia on prostate cancer progression and metastasis.Molecular biology reports · 2023Review
- HDAC1 disrupts the tricarboxylic acid (TCA) cycle through the deacetylation of Nur77 and promotes inflammation in ischemia-reperfusion mice.Cell death discovery · 2023Article
- NR4A1 inhibits the epithelial-mesenchymal transition of hepatic stellate cells: Involvement of TGF-β-Smad2/3/4-ZEB signaling.Open life sciences · 2022Article
- Therapeutic potential of NR4A1 in cancer: Focus on metabolism.Frontiers in oncology · 2022Review
- Nur77 Attenuates Inflammasome Activation by Inhibiting Caspase-1 Expression in Pulmonary Vascular Endothelial Cells.American journal of respiratory cell and molecular biology · 2021Article
- Transcriptomic analysis of the mouse retina after acute and chronic normobaric and hypobaric hypoxia.Scientific reports · 2021Article
- The effect of intermittent hypoxia and fecal microbiota of OSAS on genes associated with colorectal cancer.Sleep & breathing = Schlaf & Atmung · 2021Article
- Interplay between transforming growth factor-β and Nur77 in dual regulations of inhibitor of differentiation 1 for colonic tumorigenesis.Nature communications · 2021Article
- Targeting NR4A Nuclear Receptors to Control Stromal Cell Inflammation, Metabolism, Angiogenesis, and Tumorigenesis.Frontiers in cell and developmental biology · 2021Review
- Hypoxia-induced Nur77 activates PI3K/Akt signalingTheranostics · 2021Article
- β-glucan from Lentinus edodes inhibits breast cancer progression via the Nur77/HIF-1α axis.Bioscience reports · 2020Article
- Bis-indole derived nuclear receptor 4A1 (NR4A1) antagonists inhibit TGFβ-induced invasion of embryonal rhabdomyosarcoma cells.American journal of cancer research · 2020Article
- Nur77 limits endothelial barrier disruption to LPS in the mouse lung.American journal of physiology. Lung cellular and molecular physiology · 2019Article
- Expression Signatures of Cisplatin- and Trametinib-Treated Early-Stage Medaka Melanomas.G3 (Bethesda, Md.) · 2019Article
- MiR-506 Suppresses Colorectal Cancer Development by Inhibiting Orphan Nuclear Receptor NR4A1 Expression.Journal of Cancer · 2019Article
- Characteristics of Nur77 and its ligands as potential anticancer compounds (Review).Molecular medicine reports · 2018Review
- Overexpression of NR4A1 is associated with tumor recurrence and poor survival in non-small-cell lung carcinoma.Oncotarget · 2017Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundβ-Catenin is a potent oncogenic protein in colorectal cancer (CRC), but the targets and regulation of this important signalling molecule are not completely understood. Hypoxia is a prominent feature of solid tumours that contributes to cancer progression.
methodsHere, we analysed the regulation between Nur77 and β-catenin under hypoxic conditions. Cell proliferation, migration, and invasion assays were performed to assess functional consequences.
resultsWe showed that hypoxia stimulated co-upregulation of β-catenin and Nur77 in a number of human CRC cell lines. Interestingly, expression of β-catenin and Nur77 by hypoxia formed a mutual feedback regulation circuits that conferred aggressive growth of CRC. Overexpression of β-catenin increased Nur77 transcription through hypoxia-inducible factor-1α rather than T-cell factor. Nur77-mediated activation of β-catenin by hypoxia was independent of both DNA binding and transactivation. Further, we showed that hypoxic activation of β-catenin was independent of the classical adenomatous polyposis coli and p53 pathways, but stimulated by phosphatidylinositol 3-kinase/Akt in a Nur77-dependent manner. Under hypoxic conditions, enhanced β-catenin and Nur77 expression synergistically stimulated CRC cell migration, invasion, and epithelial-mesenchymal transition.
conclusionThese findings provide a novel molecular mechanism for hypoxic CRCs that may contribute to tumour progression, and its targeting may represent an effective therapeutic avenue.
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