ArticleCell cycle (Georgetown, Tex.)2011
Antagonistic crosstalk between APC and HIF-1α.
Article in Cell cycle (Georgetown, Tex.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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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
10 citing papers in PubMed, 18 citations in OpenAlex.
- Multi-omics exploration of hypoxia in gastric cancer.World journal of surgical oncology · 2026Article
- The role of oxygen tension in cell fate and regenerative medicine: implications of hypoxia/hyperoxia and free radicals.Cell and tissue banking · 2024Review
- Targeting Wnt/β-Catenin Pathways in Primary Liver Tumours: From Microenvironment Signaling to Therapeutic Agents.Cancers · 2022Review
- Transmembrane Protein 100 Inhibits the Progression of Colorectal Cancer by Promoting the Ubiquitin/Proteasome Degradation of HIF-1α.Frontiers in oncology · 2022Article
- Article
- Liver Zonation in Health and Disease: Hypoxia and Hypoxia-Inducible Transcription Factors as Concert Masters.International journal of molecular sciences · 2019Review
- Hypoxia and Inflammation in Cancer, Focus on HIF and NF-κB.Biomedicines · 2017Review
- Metabolic zonation of the liver: The oxygen gradient revisited.Redox biology · 2017Review
- The role of hypoxia in inflammatory disease (review).International journal of molecular medicine · 2015Review
- HAF drives the switch of HIF-1α to HIF-2α by activating the NF-κB pathway, leading to malignant behavior of T24 bladder cancer cells.International journal of oncology · 2014Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Most colorectal cancers have mutations in the tumor suppressor APC. The best-understood function of APC is its participation in a protein complex that regulates the availability of β-catenin. Solid tumors are characterized by the presence of hypoxia as well as inflammation, which leads to the upregulation of Hypoxia Inducible Factors like HIF-1α. We recently demonstrated a novel antagonistic link between APC and HIF-1α. We found that hypoxia results in reduced levels of APC mRNA and protein via a direct HIF-1α-dependent mechanism. Similarly, APC mediates the repression of HIF-1α. However, this requires wild-type APC, low levels of β-catenin and NFκB activity. These results reveal the downregulation of APC as a novel mechanism that contributes to the survival advantage induced by hypoxia and cytokines such as TNFα. Our data indicate that loss-of-function mutations in APC result in the engagement of the hypoxia response. Importantly, this suggests that other stimuli that induce HIF, such as inflammatory cytokines and oncogenes, alter APC function.
Indexed as
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What OpenQuestion holds
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.