ArticleCarcinogenesis2013
Hypoxia-inducible factor-2α is essential in activating the COX2/mPGES-1/PGE2 signaling axis in colon cancer.
Article in Carcinogenesis, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 74 citations in OpenAlex.
- Uric Acid Induces Hepatocytes Ferroptosis Through HIF-2α/DMT1-Mediated Iron Overload.International journal of molecular sciences · 2026Article
- Beyond Iron Solubility: Particle Size as a Determinant of Cell Survival and Iron-Induced COX-2 Expression in Human Intestinal Cells.Biomolecules · 2026Article
- Targeting HIF-2α in colorectal cancer reveals a cholesterol biosynthesis-dependent ferroptotic vulnerability.Cancer & metabolism · 2026Article
- Targeting HIF-2α in Colorectal Cancer Reveals a Cholesterol Biosynthesis-Dependent Ferroptotic Vulnerability.bioRxiv : the preprint server for biology · 2026Article
- Obstructive sleep apnea and lung cancer: molecular underpinnings and clinical translational prospects.Frontiers in cell and developmental biology · 2026Review
- The Gut Microbiota-Ferroptosis Axis: Emerging Perspectives in Gastrointestinal Tumorigenesis and Progression.Current issues in molecular biology · 2025Review
- Rel Family Transcription Factor NFAT5 Upregulates COX2 via HIF-1α Activity in Ishikawa and HEC1a Cells.International journal of molecular sciences · 2024Article
- Hypoxia-Induced Signaling in Gut and Liver Pathobiology.Annual review of pathology · 2024Review
- High hypoxia status in pancreatic cancer is associated with multiple hallmarks of an immunosuppressive tumor microenvironment.Frontiers in immunology · 2024Article
- Iron promotes glycolysis to drive colon tumorigenesis.Biochimica et biophysica acta. Molecular basis of disease · 2023Article
- Prostaglandin E2 Exposure Disrupts E-Cadherin/Caveolin-1-Mediated Tumor Suppression to Favor Caveolin-1-Enhanced Migration, Invasion, and Metastasis in Melanoma Models.International journal of molecular sciences · 2023Article
- Hypoxia in the Pathophysiology of Inflammatory Bowel Disease.Comprehensive Physiology · 2023Article
- PTGES Expression Is Associated with Metabolic and Immune Reprogramming in Pancreatic Ductal Adenocarcinoma.International journal of molecular sciences · 2023Article
- A pleiotropic hypoxia-sensitiveScience advances · 2022Article
- Exploring Nitric Oxide (NO)-Releasing Celecoxib Derivatives as Modulators of Radioresponse in Pheochromocytoma Cells.Molecules (Basel, Switzerland) · 2022Article
- Review
- Hypoxia signaling in human health and diseases: implications and prospects for therapeutics.Signal transduction and targeted therapy · 2022Review
- The hypoxia-inducible factor prolyl hydroxylase inhibitor FG4592 promotes natriuresis through upregulation of COX2 in the renal medulla.Hypertension research : official journal of the Japanese Society of Hypertension · 2022Article
- A small molecule HIF-1α stabilizer that accelerates diabetic wound healing.Nature communications · 2021Article
- The effect of intermittent hypoxia and fecal microbiota of OSAS on genes associated with colorectal cancer.Sleep & breathing = Schlaf & Atmung · 2021Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Cyclooxygenase 2 (COX2) is overexpressed in 80% of colon adenocarcinomas. However, the mechanism leading to aberrant COX2 expression in tumors is unclear. Intestinal epithelium-specific disruption of the von Hippel-Lindau tumor suppressor protein (VHL) in adenomatous polyposis coli (Apc)(min/+) mice (Vhl(ΔIE)/Apc(min/+)) resulted in constitutive activation of hypoxia-inducible factor (HIF), robustly enhanced colon carcinogenesis and potentiated COX2 expression in normal colon epithelium and tumors. In this study, we hypothesize that HIF regulates COX2 expression in colon tumors, and this regulation is critical for HIF-mediated colon carcinogenesis. COX2 was demonstrated to be a direct target gene of HIF-2α, and genetic disruption of HIF-2α abolished the induction of COX2 in tumors. Furthermore, inhibition of COX2 by nimesulide reduced HIF-2α-induced colon tumor formation. Interestingly, the levels of prostaglandin E(2) (PGE(2)), the downstream effector of COX2, remained elevated in normal and tumor tissues of the nimesulide-treated Vhl(ΔIE)/Apc(min/+) mice. Further examination revealed that the terminal PGE(2) synthesis enzyme microsomal prostaglandin E synthase 1 (mPGES-1) was overexpressed in the colon of Vhl(ΔIE)/Apc(min/+) mice. mPGES-1 was demonstrated to be a direct target gene of HIF-2α, and genetic disruption of HIF-2α abolished the induction of mPGES-1 in colon tumors. Together, our findings demonstrate that HIF-2α is a major regulator of COX2/mPGES-1/PGE(2) pathway in colon tumors.
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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.