ArticleOncogene2013
Identification of pY654-β-catenin as a critical co-factor in hypoxia-inducible factor-1α signaling and tumor responses to hypoxia.
Article in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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Who cites it
23 citing papers in PubMed, 35 citations in OpenAlex.
- NOX1 and PRDX6 synergistically support migration and invasiveness of hepatocellular carcinoma cells through enhanced NADPH oxidase activity.Advances in redox research · 2023Article
- A reversible SRC-relayed COX2 inflammatory program drives resistance to BRAF and EGFR inhibition in BRAFNature cancer · 2023Article
- Phosphorylation-Dependent Regulation of WNT/Beta-Catenin Signaling.Frontiers in oncology · 2022Review
- Advanced glycation end products induce endothelial hyperpermeability via β-catenin phosphorylation and subsequent up-regulation of ADAM10.Journal of cellular and molecular medicine · 2021Article
- Mucosal Epithelial Jak Kinases in Health and Diseases.Mediators of inflammation · 2021Review
- Development and Validation of an Mesenchymal-Related Long Non-Coding RNA Prognostic Model in Glioma.Frontiers in oncology · 2021Article
- Inhibition of Carbonyl Reductase 1 Enhances Metastasis of Head and Neck Squamous Cell Carcinoma through β-catenin-Mediated Epithelial-Mesenchymal Transition.Journal of Cancer · 2020Article
- β‑catenin nuclear translocation induced by HIF‑1α overexpression leads to the radioresistance of prostate cancer.International journal of oncology · 2018Article
- A Shared Pattern of β-Catenin Activation in Bronchopulmonary Dysplasia and Idiopathic Pulmonary Fibrosis.The American journal of pathology · 2018Article
- Signaling pathways and mesenchymal transition in pediatric high-grade glioma.Cellular and molecular life sciences : CMLS · 2018Review
- Long noncoding RNA NORAD, a novel competing endogenous RNA, enhances the hypoxia-induced epithelial-mesenchymal transition to promote metastasis in pancreatic cancer.Molecular cancer · 2017Article
- Janus kinase 3 regulates adherens junctions and epithelial mesenchymal transition through β-catenin.The Journal of biological chemistry · 2017Article
- Hypoxia-Inducible Factor 1α Signaling Promotes Repair of the Alveolar Epithelium after Acute Lung Injury.The American journal of pathology · 2017Article
- Article
- Hypoxia-induced modulation of PTEN activity and EMT phenotypes in lung cancers.Cancer cell international · 2016Article
- Reactive Oxygen Species and Targeted Therapy for Pancreatic Cancer.Oxidative medicine and cellular longevity · 2016Review
- Nuclear signaling from cadherin adhesion complexes.Current topics in developmental biology · 2015Review
- Bioinformatic approaches to augment study of epithelial-to-mesenchymal transition in lung cancer.Physiological genomics · 2014Review
- Utility of a bacterial infection model to study epithelial-mesenchymal transition, mesenchymal-epithelial transition or tumorigenesis.Oncogene · 2014Article
- Enhanceosomes as integrators of hypoxia inducible factor (HIF) and other transcription factors in the hypoxic transcriptional response.Cellular signalling · 2013Review
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Hypoxia is linked to epithelial-mesenchymal transition (EMT) and tumor progression in numerous carcinomas. Responses to hypoxia are thought to operate via hypoxia-inducible factors (HIFs), but the importance of co-factors that regulate HIF signaling within tumors is not well understood. Here, we elucidate a signaling pathway that physically and functionally couples tyrosine phosphorylation of β-catenin to HIF1α signaling and HIF1α-mediated tumor EMT. Primary human lung adenocarcinomas accumulate pY654-β-catenin and HIF1α. All pY654-β-catenin, and only the tyrosine phosphorylated form, was found complexed with HIF1α and active Src, both within the human tumors and in lung tumor cell lines exposed to hypoxia. Phosphorylation of Y654, generated by hypoxia mediated, reactive oxygen species (ROS)-dependent Src kinase activation, was required for β-catenin to interact with HIF1α and Src, to promote HIF1α transcriptional activity, and for hypoxia-induced EMT. Mice bearing hypoxic pancreatic islet adenomas, generated by treatment with anti-vascular endothelial growth factor antibodies, accumulate HIF1α/pY654-β-catenin complexes and develop an invasive phenotype. Concurrent administration of the ROS inhibitor N-acetylcysteine abrogated β-catenin/HIF pathway activity and restored adenoma architecture. Collectively, the findings implicate accumulation of pY654-β-catenin specifically complexed to HIF1α and Src kinase as critically involved in HIF1α signaling and tumor invasion. The findings also suggest that targeting ROS-dependent aspects of the pY654-β-catenin/ HIF1α pathway may attenuate untoward biological effects of anti-angiogenic agents and tumor hypoxia.
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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.