ReviewJournal of bioenergetics and biomembranes2012
Regulation of metastasis; mitochondrial DNA mutations have appeared on stage.
Review in Journal of bioenergetics and biomembranes, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 19 citations in OpenAlex.
- Cytochrome c Oxidase Subunit COX4-1 Reprograms Erastin-Induced Cell Death from Ferroptosis to Apoptosis: A Transmitochondrial Study.Antioxidants (Basel, Switzerland) · 2025Article
- Targeting Mitochondrial Function with Chemoptogenetics.Biomedicines · 2022Review
- Review
- Suppression of non-small-cell lung cancer A549 tumor growth by an mtDNA mutation-targeting pyrrole-imidazole polyamide-triphenylphosphonium and a senolytic drug.Cancer science · 2022Article
- The Role of Mitochondria in Carcinogenesis.International journal of molecular sciences · 2021Review
- Mitochondrion: I am more than a fuel server.Annals of translational medicine · 2019Review
- Article
- mtDNA, Metastasis, and the Mitochondrial Unfolded Protein Response (UPRFrontiers in cell and developmental biology · 2017Review
- A Comprehensive Characterization of Mitochondrial Genome in Papillary Thyroid Cancer.International journal of molecular sciences · 2016Article
- Decoding Warburg's hypothesis: tumor-related mutations in the mitochondrial respiratory chain.Oncotarget · 2015Review
- Circulating mitochondrial DNA content associated with the risk of liver cirrhosis: a nested case-control study.Digestive diseases and sciences · 2015Article
- Stat3: friend or foe in colitis and colitis-associated cancer?Inflammatory bowel diseases · 2014Review
- The mitochondrial ATPase6 gene is more susceptible to mutation than the ATPase8 gene in breast cancer patients.Cancer cell international · 2014Article
- How does the metabolism of tumour cells differ from that of normal cells.Bioscience reports · 2013Review
- Mitochondria in relation to cancer metastasis: introduction to a mini-review series.Journal of bioenergetics and biomembranes · 2012Article
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 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It has been controversial whether mtDNA mutations are responsible for tumorigenesis and for the process to develop metastases. To clarify this issue, we established trans-mitochondrial cybrids with mtDNA exchanged between mouse tumor cells that possess high and low metastatic potential. The results revealed that the G13997A mutation in the ND6 gene of mtDNA from highly metastatic tumor cells reversibly controlled development of metastases by overproduction of reactive oxygen species (ROS). The transmitochondrial model mice possessing G13997A mtDNA showed symptoms of impaired glucose tolerability, suggesting that ROS generated mtDNA mutations can regulate not only metastatic potential, but also age-associated disorders such as diabetes. We also identified other mtDNA mutations that affect metastatic potential but the mechanisms are independent of ROS production. The mtDNA-mediated reversible control of metastasis and age-associated disorders are novel functions of mtDNA, and suggests that ROS scavengers may be therapeutically effective to suppress these phenotypes.
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.