ArticleJournal of carcinogenesis2009
p53 regulates mtDNA copy number and mitocheckpoint pathway.
Article in Journal of carcinogenesis, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.
What it found
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Who cites it
73 citing papers in PubMed, 139 citations in OpenAlex.
- Metabolic control analysis of cellular respiration in situ in intraoperational samples of human breast cancer.Journal of bioenergetics and biomembranes · 2012Trial
- Dynamics of mitochondrial DNA copy number regulation in relation to gastric cancer survival.Discover oncology · 2025Article
- CHCHD4 Oxidoreductase Activity: A Comprehensive Analysis of the Molecular, Functional, and Structural Properties of Its Redox-Regulated Substrates.Molecules (Basel, Switzerland) · 2025Review
- The Role of p53 Mutations in Early and Late Response to Mitotic Aberrations.Biomolecules · 2025Review
- Revisiting the Role of Mitochondrial DNA Mutations in Aging: Bridging Theoretical Expectations with Empirical Observations.Aging and disease · 2025Review
- Aging through the lens of mitochondrial DNA mutations and inheritance paradoxes.Biogerontology · 2024Review
- Loss-of-function mitochondrial DNA polymerase gamma variants cause vascular smooth muscle cells to secrete a diffusible mitogenic factor.Frontiers in physiology · 2024Article
- The Role of Genetic Mutations in Mitochondrial-Driven Cancer Growth in Selected Tumors: Breast and Gynecological Malignancies.Life (Basel, Switzerland) · 2023Review
- Yeast Chromatin Mutants Reveal Altered mtDNA Copy Number and Impaired Mitochondrial Membrane Potential.Journal of fungi (Basel, Switzerland) · 2023Article
- Peripheral blood leukocyte mitochondrial DNA content and risk of lung cancer.Translational lung cancer research · 2022Article
- Mitochondrial DNA copy number in cervical exfoliated cells and risk of cervical cancer among HPV-positive women.BMC women's health · 2020Article
- Mitochondria-hubs for regulating cellular biochemistry: emerging concepts and networks.Open biology · 2019Article
- Micromanaging aerobic respiration and glycolysis in cancer cells.Molecular metabolism · 2019Review
- d-amino acid oxidase promotes cellular senescence via the production of reactive oxygen species.Life science alliance · 2019Article
- Colorectal Cancer and Metabolism.Current colorectal cancer reports · 2018Article
- p53-inducible DPYSL4 associates with mitochondrial supercomplexes and regulates energy metabolism in adipocytes and cancer cells.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Mitochondrial dysfunction suppresses p53 expression via calcium-mediated nuclear factor-kB signaling in HCT116 human colorectal carcinoma cells.BMB reports · 2018Article
- Emerging Roles of p53 Family Members in Glucose Metabolism.International journal of molecular sciences · 2018Review
- Defining the momiome: Promiscuous information transfer by mobile mitochondria and the mitochondrial genome.Seminars in cancer biology · 2017Review
- Mitochondrial determinants of cancer health disparities.Seminars in cancer biology · 2017Review
13 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundWe previously hypothesized a role for mitochondria damage checkpoint (mito-checkpoint) in maintaining the mitochondrial integrity of cells. Consistent with this hypothesis, defects in mitochondria have been demonstrated to cause genetic and epigenetic changes in the nuclear DNA, resistance to cell-death and tumorigenesis. In this paper, we describe that defects in mitochondria arising from the inhibition of mitochondrial oxidative phosphorylation (mtOXPHOS) induce cell cycle arrest, a response similar to the DNA damage checkpoint response. MATERIALS AND
methodsPrimary mouse embryonic fibroblasts obtained from p53 wild-type and p53-deficient mouse embryos (p53 -/-) were treated with inhibitors of electron transport chain and cell cycle analysis, ROS production, mitochondrial content analysis and immunoblotting was performed. The expression of p53R2 was also measured by real time quantitative PCR.
resultsWe determined that, while p53 +/+ cells arrest in the cell cycle, p53 -/- cells continued to divide after exposure to mitochondrial inhibitors, showing that p53 plays an important role in the S-phase delay in the cell cycle. p53 is translocated to mitochondria after mtOXPHOS inhibition. Our study also revealed that p53-dependent induction of reactive oxygen species acts as a major signal triggering a mito-checkpoint response. Furthermore our study revealed that loss of p53 results in down regulation of p53R2 that contributes to depletion of mtDNA in primary MEF cells.
conclusionsOur study suggests that p53 1) functions as mito-checkpoint protein and 2) regulates mtDNA copy number and mitochondrial biogenesis. We describe a conceptual organization of the mito-checkpoint pathway in which identified roles of p53 in mitochondria are incorporated.
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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.