ArticleOncogene2000
Redox regulation of p53 during hypoxia.
Article in Oncogene, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 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
63 citing papers in PubMed, 155 citations in OpenAlex.
- p53 and TIGAR promote redox control to protect against metabolic dysfunction-associated steatohepatitis.JHEP reports : innovation in hepatology · 2025Article
- Article
- Review
- Role of mitochondrial reactive oxygen species in homeostasis regulation.Redox report : communications in free radical research · 2022Review
- Transcriptional Repression of Aerobic Glycolysis by OVOL2 in Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- ROS-Related miRNAs Regulate Immune Response and Chemoradiotherapy Sensitivity in Hepatocellular Carcinoma by Comprehensive Analysis and Experiment.Oxidative medicine and cellular longevity · 2022Article
- A microtubule-localizing activity-based sensing fluorescent probe for imaging hydrogen peroxide in living cells.Bioorganic & medicinal chemistry letters · 2021Article
- Mitochondrial transplantation in cardiomyocytes: foundation, methods, and outcomes.American journal of physiology. Cell physiology · 2021Review
- Metabolic Control by DNA Tumor Virus-Encoded Proteins.Pathogens (Basel, Switzerland) · 2021Review
- Novel Functions of CD147 in the Mitochondria Exacerbates Melanoma Metastasis.International journal of biological sciences · 2021Article
- ROS Pleiotropy in Melanoma and Local Therapy with Physical Modalities.Oxidative medicine and cellular longevity · 2021Review
- The Interplay Between Tumor Suppressor p53 and Hypoxia Signaling Pathways in Cancer.Frontiers in cell and developmental biology · 2021Review
- The Effects of Continuous and Withdrawal Voluntary Wheel Running Exercise on the Expression of Senescence-Related Genes in the Visceral Adipose Tissue of Young Mice.International journal of molecular sciences · 2020Article
- Metabolic ROS Signaling: To Immunity and Beyond.Biochemistry. Biokhimiia · 2020Review
- Resveratrol and Tumor Microenvironment: Mechanistic Basis and Therapeutic Targets.Molecules (Basel, Switzerland) · 2020Review
- Metabolic functions of the tumor suppressor p53: Implications in normal physiology, metabolic disorders, and cancer.Molecular metabolism · 2020Review
- Intracellular redox potential is correlated with miRNA expression in MCF7 cells under hypoxic conditions.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Comparative Assessment of Tungsten Toxicity in the Absence or Presence of Other Metals.Toxics · 2018Review
- Idiopathic Pulmonary Fibrosis: Aging, Mitochondrial Dysfunction, and Cellular Bioenergetics.Frontiers in medicine · 2018Review
- Oxidation-Responsive, EuACS omega · 2017Article
3 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The transcription factor p53 can induce growth arrest or death in cells. Tumor cells that develop mutations in p53 demonstrate a diminished apoptotic potential, which may contribute to growth and tumor metastasis. Cellular levels of p53 are stabilized during hypoxia. The present study tested the hypothesis that reactive oxygen species (ROS) released from mitochondria regulate the cytosolic redox state and are required for the stabilization of p53 protein levels in response to hypoxia. Our results indicate that hypoxia (1.5% O2) increases mitochondrial ROS generation and increases p53 protein levels in human breast carcinoma MCF-7 cells and in normal human diploid fibroblast IMR-90 cells. MCF-7 cells depleted of their mitochondrial DNA (rho(o) cells) failed to stabilize p53 protein levels during hypoxia. The antioxidant N-acetylcysteine and the Cu/Zn superoxide dismutase inhibitor diethyldithiocarbamic acid abolished the hypoxia-induced increases in ROS and p53 levels. Rotenone, an inhibitor of mitochondrial complex I, and 4,4'-diisothiocyanato-stilbene-2,2'-disulfonate, a mitochondrial anion channel inhibitor, also abolished the increase in ROS signal and p53 levels during hypoxia. The p53-dependent gene p21WAF1/CIP1 was also induced by hypoxia in both MCF-7 and IMR-90 cells without affecting the growth rate of either cell line. In contrast, both cell lines exhibited increases in p21WAF1/CIP1 expression and growth arrest after gamma irradiation. Primary chick cardiac myocytes and murine embryonic fibroblasts also showed an increase in p53 protein levels in response to hypoxia without cell death or growth arrest. These results indicate that mitochondria regulate p53 protein levels during hypoxia through a redox-dependent mechanism involving ROS. Despite p53-induction, hypoxia alone does not cause either growth arrest or cell death.
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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.