ArticleThe Journal of clinical investigation2009
HIF2alpha cooperates with RAS to promote lung tumorigenesis in mice.
Article in The Journal of clinical investigation, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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
84 citing papers in PubMed, 1 synthesis or guideline pooled it, 139 citations in OpenAlex.
- A regulation probability model-based meta-analysis of multiple transcriptomics data sets for cancer biomarker identification.BMC bioinformatics · 2017Pooled it
- Normoxic HIFα-mediated metabolic rewiring in cancer as a novel therapeutic target of tumor heterogeneity.Cancer & metabolism · 2026Article
- HIF2α negatively regulates MYCN protein levels and promotes a low-risk noradrenergic phenotype in neuroblastoma.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- HIF2α-dependent Dock4/Rac1-signaling regulates formation of adherens junctions and cell polarity in normoxia.Scientific reports · 2024Article
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- Lung Cancer Gene Regulatory Network of Transcription Factors Related to the Hallmarks of Cancer.Current issues in molecular biology · 2023Article
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- Stromal HIF2 Regulates Immune Suppression in the Pancreatic Cancer Microenvironment.Gastroenterology · 2022Article
- Prolonged hypoxia switched on cancer stem cell-like plasticity in HepG2 tumourspheres cultured in serum-free media.In vitro cellular & developmental biology. Animal · 2021Article
- Mild chronic hypoxia-induced HIF-2α interacts with c-MYC through competition with HIF-1α to induce hepatocellular carcinoma cell proliferation.Cellular oncology (Dordrecht, Netherlands) · 2021Article
- Hypoxia-Driven Effects in Cancer: Characterization, Mechanisms, and Therapeutic Implications.Cells · 2021Review
- Mimicking Tumor Hypoxia in Non-Small Cell Lung Cancer Employing Three-Dimensional In Vitro Models.Cells · 2021Review
- HIF-1α Metabolic Pathways in Human Cancer.Advances in experimental medicine and biology · 2021Review
- SIPA1 Enhances Aerobic Glycolysis Through HIF-2α Pathway to Promote Breast Cancer Metastasis.Frontiers in cell and developmental biology · 2021Article
- Artesunate inhibits epithelial-mesenchymal transition in non-small-cell lung cancer (NSCLC) cells by down-regulating the expression ofBioengineered · 2020Article
- Hypoxia-Induced Epithelial-Mesenchymal Transition in Cancers: HIF-1α and Beyond.Frontiers in oncology · 2020Review
- Metabolic Remodelling: An Accomplice for New Therapeutic Strategies to Fight Lung Cancer.Antioxidants (Basel, Switzerland) · 2019Review
- The Atypical Receptor CCRL2 Is Essential for Lung Cancer Immune Surveillance.Cancer immunology research · 2019Article
- H19-Dependent Transcriptional Regulation of β3 and β4 Integrins Upon Estrogen and Hypoxia Favors Metastatic Potential in Prostate Cancer.International journal of molecular sciences · 2019Article
24 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
20 authors at 5 institutions in 1 country.
Funding
Abstract
Members of the hypoxia-inducible factor (HIF) family of transcription factors regulate the cellular response to hypoxia. In non-small cell lung cancer (NSCLC), high HIF2alpha levels correlate with decreased overall survival, and inhibition of either the protein encoded by the canonical HIF target gene VEGF or VEGFR2 improves clinical outcomes. However, whether HIF2alpha is causal in imparting this poor prognosis is unknown. Here, we generated mice that conditionally express both a nondegradable variant of HIF2alpha and a mutant form of Kras (KrasG12D) that induces lung tumors. Mice expressing both Hif2a and KrasG12D in the lungs developed larger tumors and had an increased tumor burden and decreased survival compared with mice expressing only KrasG12D. Additionally, tumors expressing both KrasG12D and Hif2a were more invasive, demonstrated features of epithelial- mesenchymal transition (EMT), and exhibited increased angiogenesis associated with mobilization of circulating endothelial progenitor cells. These results implicate HIF2alpha causally in the pathogenesis of lung cancer in mice, demonstrate in vivo that HIF2alpha can promote expression of markers of EMT, and define HIF2alpha as a promoter of tumor growth and progression in a solid tumor other than renal cell carcinoma. They further suggest a possible causal relationship between HIF2alpha and prognosis in patients with NSCLC.
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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.