ArticlePloS one2014
The role of the HIF-1α transcription factor in increased cell division at physiological oxygen tensions.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 32 citations in OpenAlex.
- Enhancing the efficacy of VEGF inhibitors by co-inhibition of HIF in the treatment of glioblastoma.Apoptosis : an international journal on programmed cell death · 2026Review
- The Physiological Functions and Therapeutic Potential of Hypoxia-Inducible Factor-1α in Vascular Calcification.Biomolecules · 2024Review
- Four Markers Useful for the Distinction of Intrauterine Growth Restriction in Sheep.Animals : an open access journal from MDPI · 2023Article
- USP10 Contributes to Colon Carcinogenesis via mTOR/S6K Mediated HIF-1α but Not HIF-2α Protein Synthesis.Cells · 2023Article
- Modeling Preclinical Cancer Studies under Physioxia to Enhance Clinical Translation.Cancer research · 2022Review
- In Vitro Angiogenesis Inhibition and Endothelial Cell Growth and Morphology.International journal of molecular sciences · 2022Article
- A distinctive distribution of hypoxia-inducible factor-1α in cultured renal tubular cells with hypoperfusion simulated by coverslip placement.Physiological reports · 2021Article
- Amelioration of age-related brain function decline by Bruton's tyrosine kinase inhibition.Aging cell · 2020Article
- The role of hypoxic signalling in metastasis: towards translating knowledge of basic biology into novel anti-tumour strategies.Clinical & experimental metastasis · 2018Review
- Physiological Hypoxia (Physioxia) Impairs the Early Adhesion of Single Lymphoma Cell to Marrow Stromal Cell and Extracellular Matrix. Optical Tweezers Study.International journal of molecular sciences · 2018Article
- Endothelial HIF-2α contributes to severe pulmonary hypertension due to endothelial-to-mesenchymal transition.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- BTK modulates p73 activity to induce apoptosis independently of p53.Cell death discovery · 2018Article
- BTK blocks the inhibitory effects of MDM2 on p53 activity.Oncotarget · 2017Article
- Modeling tumor cell adaptations to hypoxia in multicellular tumor spheroids.Journal of experimental & clinical cancer research : CR · 2017Review
- Current relevance of hypoxia in head and neck cancer.Oncotarget · 2016Review
- Cell cycle progression in glioblastoma cells is unaffected by pathophysiological levels of hypoxia.PeerJ · 2016Article
- The twisted survivin connection to angiogenesis.Molecular cancer · 2015Review
- Hypoxia Inducible Factor Pathway and Physiological Adaptation: A Cell Survival Pathway?Mediators of inflammation · 2015Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
HIF-1 is a transcription factor that mediates the cellular responses to low oxygen environments, mainly as a result of having an oxygen-labile subunit, HIF-1α. HIF-1α has been carefully studied in the context of severe hypoxic stresses (<1% O2), but it is also known to be present at oxygen tensions commonly found in normal tissues in vivo (∼1-13% O2), albeit at much lower levels. Its role under these physiological conditions is not fully understood. Here, we show that a transcriptionally active HIF-1α was up-regulated at 5% O2, both in normal and cancer cells, but only some of its target genes were elevated as a result. HIF-1α induction was in part dependent on the activation of the ERK1/2 MAPK signalling pathway, which we have previously shown is active at 5% O2. We also found that HIF-1α does not contribute to the protection against DNA damage that can be observed in low oxygen environments, and that there are certain DNA damaging agents, such as doxorubicin and actinomycin D, that prevent HIF-1α induction independently of p53. Moreover, absence of HIF-1α significantly reduced the growth advantage of cells cultured at 5% O2. In view of these data, we conclude that HIF-1α can be induced and activated at physiological oxygen tensions in a MAPK-dependent manner and that, although this does not lead to pro-survival responses to stress, it determines the increased cell proliferation rates that are common under these conditions.
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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.