ArticleThe Journal of biological chemistry2011
Mitochondrial dysfunction impairs tumor suppressor p53 expression/function.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 61 citations in OpenAlex.
- Stress increases sperm respiration and motility in mice and men.Nature communications · 2024Article
- Mitochondrial NME6 Influences Basic Cellular Processes in Tumor Cells In Vitro.International journal of molecular sciences · 2024Article
- A dataset describing glycolytic inhibitors overcoming the underestimation of maximal mitochondrial oxygen consumption rate in oligomycin-treated cells.Data in brief · 2022Article
- Shared evolutionary footprints suggest mitochondrial oxidative damage underlies multiple complex I losses in fungi.Open biology · 2021Article
- Analysis of Mitochondrial Retrograde Signaling in Yeast Model Systems.Methods in molecular biology (Clifton, N.J.) · 2021Article
- Mechanisms of drugs-resistance in small cell lung cancer: DNA-related, RNA-related, apoptosis-related, drug accumulation and metabolism procedure.Translational lung cancer research · 2020Review
- Mapping mitochondrial respiratory chain deficiencies by respirometry: Beyond the Mito Stress Test.Experimental neurology · 2020Article
- Anti-senescence role of heterozygous fumarate hydratase gene knockout in rat lung fibroblastsAging · 2019Article
- Widespread Chromosomal Losses and Mitochondrial DNA Alterations as Genetic Drivers in Hürthle Cell Carcinoma.Cancer cell · 2018Article
- Early loss of mitochondrial complex I and rewiring of glutathione metabolism in renal oncocytoma.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Epigenetic modification of miR-663 controls mitochondria-to-nucleus retrograde signaling and tumor progression.The Journal of biological chemistry · 2017Article
- Simulation of Cellular Energy Restriction in Quiescence (ERiQ)-A Theoretical Model for Aging.Biology · 2017Article
- Mitochondrial determinants of cancer health disparities.Seminars in cancer biology · 2017Review
- Individual-specific variation in the respiratory activities of HMECs and their bioenergetic response to IGF1 and TNFα.Journal of cellular physiology · 2017Article
- Oncogenes, mitochondrial metabolism, and quality control in differentiated thyroid cancer.The Korean journal of internal medicine · 2017Review
- MicroRNA-34a Encapsulated in Hyaluronic Acid Nanoparticles Induces Epigenetic Changes with Altered Mitochondrial Bioenergetics and Apoptosis in Non-Small-Cell Lung Cancer Cells.Scientific reports · 2017Article
- Downregulation of LRRC8A protects human ovarian and alveolar carcinoma cells against Cisplatin-induced expression of p53, MDM2, p21Waf1/Cip1, and Caspase-9/-3 activation.American journal of physiology. Cell physiology · 2016Article
- Article
- Oxidative phosphorylation-dependent regulation of cancer cell apoptosis in response to anticancer agents.Cell death & disease · 2015Article
- ASPP2 enhances oxaliplatin (L-OHP)-induced colorectal cancer cell apoptosis in a p53-independent manner by inhibiting cell autophagy.Journal of cellular and molecular medicine · 2015Article
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
Recently, mitochondria have been suggested to act in tumor suppression. However, the underlying mechanisms by which mitochondria suppress tumorigenesis are far from being clear. In this study, we have investigated the link between mitochondrial dysfunction and the tumor suppressor protein p53 using a set of respiration-deficient (Res(-)) mammalian cell mutants with impaired assembly of the oxidative phosphorylation machinery. Our data suggest that normal mitochondrial function is required for γ-irradiation (γIR)-induced cell death, which is mainly a p53-dependent process. The Res(-) cells are protected against γIR-induced cell death due to impaired p53 expression/function. We find that the loss of complex I biogenesis in the absence of the MWFE subunit reduces the steady-state level of the p53 protein, although there is no effect on the p53 protein level in the absence of the ESSS subunit that is also essential for complex I assembly. The p53 protein level was also reduced to undetectable levels in Res(-) cells with severely impaired mitochondrial protein synthesis. This suggests that p53 protein expression is differentially regulated depending upon the type of electron transport chain/respiratory chain deficiency. Moreover, irrespective of the differences in the p53 protein expression profile, γIR-induced p53 activity is compromised in all Res(-) cells. Using two different conditional systems for complex I assembly, we also show that the effect of mitochondrial dysfunction on p53 expression/function is a reversible phenomenon. We believe that these findings will have major implications in the understanding of cancer development and therapy.
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