ReviewFrontiers in oncology2017
The Mitochondrial Complex(I)ty of Cancer.
Review in Frontiers in oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 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
101 citing papers in PubMed.
- Trial
- Glycerol enhances mitochondrial metabolism and inflammatory response in pro-inflammatory macrophages.EMBO reports · 2026Article
- Anticancer Potential of Piericidin A1 and Derivatives Isolated From Streptomyces sp. Associated With Palythoa variabilis From Brazilian Reefs.Chemistry & biodiversity · 2026Article
- NDUFS1-Mediated Mitochondrial Complex I Activity Maintains Pancreatic Cancer Stemness by Promoting PAX2 Hypomethylation.MedComm · 2026Article
- The anticancer properties of the nanocomposite of low-nanoscale Ag nanoparticles obtained in SiOBMC pharmacology & toxicology · 2026Article
- Leveraging Consensus Docking Approaches for Human Mitochondrial Complexes I and III.Chemical research in toxicology · 2026Article
- The Anti-proliferative Effects of Anandamide and Oleamide in Glioblastoma Cell Lines Recruit Mitochondrial and PPAR-γ Receptor Modulation.Neurochemical research · 2026Article
- MCJ modulates mitochondrial ETC flux to promote lipid metabolism-driven enhancement of cell proliferation and migration.Cell death & disease · 2026Article
- Mitochondrial complex I in focus: mechanisms and therapeutic strategies of urinary system diseases.Frontiers in physiology · 2026Review
- Antitumor natural products targeting mitochondrial NADH: ubiquinone oxidoreductase (complex I): a review.Frontiers in pharmacology · 2026Review
- Mitochondrial Quality Control in Neurodegeneration and Cancer: A Common Denominator, Distinct Therapeutic Challenges.International journal of molecular sciences · 2025Review
- MitCOM-based prognostic model identifies GLUD1 as a key suppressor of glioblastoma growth and invasion through regulation of mitochondrial structure and metabolism.Cancer cell international · 2025Article
- Respiratory complex I-mediated NADMolecular oncology · 2025Article
- Article
- Modeling Krebs cycle from liver, heart and hepatoma mitochondria, supported Complex I as target for specific inhibition of cancer cell proliferation.Frontiers in oncology · 2025Article
- Demethylzeylasteral inhibits oxidative phosphorylation complex biogenesis by targeting LRPPRC in lung cancer.Journal of Cancer · 2025Article
- Laminin-α2 chain deficiency in skeletal muscle causes dysregulation of multiple cellular mechanisms.Life science alliance · 2024Article
- A Comprehensive Pan-Cancer Analysis of Cytochrome C Oxidase Assembly Factor 1 (COA1) Reveals Instrumental Role of Mitochondrial Protein Assembly in Cancer that Modulates Disease Progression and Prognostic Outcome.Cell biochemistry and biophysics · 2024Article
- Insights into Molecular Mechanisms of Anticancer Activity ofPlants (Basel, Switzerland) · 2024Article
- Proteomic Characterization of a 3D HER2+ Breast Cancer Model Reveals the Role of Mitochondrial Complex I in Acquired Resistance to Trastuzumab.International journal of molecular sciences · 2024Article
41 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.
Funding
Abstract
Recent evidence highlights that the cancer cell energy requirements vary greatly from normal cells and that cancer cells exhibit different metabolic phenotypes with variable participation of both glycolysis and oxidative phosphorylation. NADH-ubiquinone oxidoreductase (Complex I) is the largest complex of the mitochondrial electron transport chain and contributes about 40% of the proton motive force required for mitochondrial ATP synthesis. In addition, Complex I plays an essential role in biosynthesis and redox control during proliferation, resistance to cell death, and metastasis of cancer cells. Although knowledge about the structure and assembly of Complex I is increasing, information about the role of Complex I subunits in tumorigenesis is scarce and contradictory. Several small molecule inhibitors of Complex I have been described as selective anticancer agents; however, pharmacologic and genetic interventions on Complex I have also shown pro-tumorigenic actions, involving different cellular signaling. Here, we discuss the role of Complex I in tumorigenesis, focusing on the specific participation of Complex I subunits in proliferation and metastasis of cancer cells.
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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.