ReviewBiochimica et biophysica acta2011
Genetic insights into OXPHOS defect and its role in cancer.
Review in Biochimica et biophysica acta, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
88 citing papers in PubMed, 151 citations in OpenAlex.
- Analyzing mitochondrial function in human peripheral blood mononuclear cells.Analytical biochemistry · 2018Trial
- Cancer-derived lactic acid as a potential upstream contributor to tumor hypoxia.Communications biology · 2026Review
- ANOS1 Facilitated Tumorigenesis in Gastric Cancer through the Regulation of Oxidative Phosphorylation Pathway.Journal of microbiology and biotechnology · 2026Article
- MRPL37 promotes hepatocellular carcinoma progression through modulating mitochondrial energy metabolism.iScience · 2025Article
- Unveiling Metabolic Subtypes in Endometrial Cancer Cell Lines: Insights from Metabolomic Analysis Under Standard and Stress Conditions.International journal of molecular sciences · 2025Article
- The Pivotal Role of One-Carbon Metabolism in Neoplastic Progression During the Aging Process.Biomolecules · 2024Review
- Article
- Complex I activity in hypoxia: implications for oncometabolism.Biochemical Society transactions · 2024Review
- Mitochondrial-Stem Cell Connection: Providing Additional Explanations for Understanding Cancer.Metabolites · 2024Article
- Oxygen and Iron Availability Shapes Metabolic Adaptations of Cancer Cells.World journal of oncology · 2024Review
- Compensatory cross-talk between autophagy and glycolysis regulates senescence and stemness in heterogeneous glioblastoma tumor subpopulations.Acta neuropathologica communications · 2023Article
- Viability of HepG2 and MCF-7 cells is not correlated with mitochondrial bioenergetics.Scientific reports · 2023Article
- The Role of Genetic Mutations in Mitochondrial-Driven Cancer Growth in Selected Tumors: Breast and Gynecological Malignancies.Life (Basel, Switzerland) · 2023Review
- STAT proteins in cancer: orchestration of metabolism.Nature reviews. Cancer · 2023Review
- Androgen receptor signaling-mitochondrial DNA-oxidative phosphorylation: A critical triangle in early prostate cancer.Current urology · 2022Article
- Organelle-targeted therapies: a comprehensive review on system design for enabling precision oncology.Signal transduction and targeted therapy · 2022Review
- Review
- Article
- YY1 promotes pancreatic cancer cell proliferation by enhancing mitochondrial respiration.Cancer cell international · 2022Article
- AMP-activated protein kinase β1 or β2 deletion enhances colon cancer cell growth and tumorigenesis.Acta biochimica et biophysica Sinica · 2022Article
28 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
2 authors at 1 institution in 1 country.
Funding
Abstract
Warburg proposed that cancer originates from irreversible injury to mitochondrial oxidative phosphorylation (mtOXPHOS), which leads to an increase rate of aerobic glycolysis in most cancers. However, despite several decades of research related to Warburg effect, very little is known about the underlying genetic cause(s) of mtOXPHOS impairment in cancers. Proteins that participate in mtOXPHOS are encoded by both mitochondrial DNA (mtDNA) as well as nuclear DNA. This review describes mutations in mtDNA and reduced mtDNA copy number, which contribute to OXPHOS defects in cancer cells. Maternally inherited mtDNA renders susceptibility to cancer, and mutation in the nuclear encoded genes causes defects in mtOXPHOS system. Mitochondria damage checkpoint (mitocheckpoint) induces epigenomic changes in the nucleus, which can reverse injury to OXPHOS. However, irreversible injury to OXPHOS can lead to persistent mitochondrial dysfunction inducing genetic instability in the nuclear genome. Together, we propose that "mitocheckpoint" led epigenomic and genomic changes must play a key role in reversible and irreversible injury to OXPHOS described by Warburg. These epigenetic and genetic changes underlie the Warburg phenotype, which contributes to the development of cancer.
Indexed as
Identifiers
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.