ArticleOncotarget2015
Enhanced tumorigenicity by mitochondrial DNA mild mutations.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 35 papers.
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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.
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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.
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Who cites it
35 citing papers in PubMed, 55 citations in OpenAlex.
- Mitochondrial retrograde signaling in gastric cancer: mtDNA mutations, ROS-driven NF-κB/HIF-1α activation, and Warburg effect amplification.Frontiers in physiology · 2026Review
- Somatic mtDNA mutations at intermediate levels of heteroplasmy are a source of functional heterogeneity among primary leukemic cells.Science advances · 2025Article
- The Warburg hypothesis and the emergence of the mitochondrial metabolic theory of cancer.Journal of bioenergetics and biomembranes · 2025Review
- Pathogenic mitochondrial DNA mutations inhibit melanoma metastasis.Science advances · 2024Article
- Mitochondrial-Stem Cell Connection: Providing Additional Explanations for Understanding Cancer.Metabolites · 2024Article
- Platinum iodido drugs show potential anti-tumor activity, affecting cancer cell metabolism and inducing ROS and senescence in gastrointestinal cancer cells.Communications biology · 2024Article
- Role of mitochondrial alterations in human cancer progression and cancer immunity.Journal of biomedical science · 2023Review
- The Interplay between Dysregulated Metabolism and Epigenetics in Cancer.Biomolecules · 2023Review
- The mitochondrial unfolded protein response (UPRJournal of hematology & oncology · 2022Review
- Mitochondrial dysfunction, UPRCell & bioscience · 2021Review
- Can the Mitochondrial Metabolic Theory Explain Better the Origin and Management of Cancer than Can the Somatic Mutation Theory?Metabolites · 2021Article
- On the Origin of ATP Synthesis in Cancer.iScience · 2020Review
- Multifaceted Roles of Mitochondrial Components and Metabolites in Metabolic Diseases and Cancer.International journal of molecular sciences · 2020Review
- Article
- Compressive Optic Neuropathy with a Concurrent Mutation of Leber's Hereditary Optic Neuropathy: A Case Report.Neuro-ophthalmology (Aeolus Press) · 2020Article
- Mitohormesis, UPRCancer research · 2019Review
- Mitochondrial Genome (mtDNA) Mutations that Generate Reactive Oxygen Species.Antioxidants (Basel, Switzerland) · 2019Review
- Mutations in theCancers · 2019Article
- Mitochondrial DNA, nuclear context, and the risk for carcinogenesis.Environmental and molecular mutagenesis · 2019Review
- Mitochondrial transplantation regulates antitumour activity, chemoresistance and mitochondrial dynamics in breast cancer.Journal of experimental & clinical cancer research : CR · 2019Article
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To understand how mitochondria are involved in malignant transformation we have generated a collection of transmitochondrial cybrid cell lines on the same nuclear background (143B) but with mutant mitochondrial DNA (mtDNA) variants with different degrees of pathogenicity. These include the severe mutation in the tRNALys gene, m.8363G>A, and the three milder yet prevalent Leber's hereditary optic neuropathy (LHON) mutations in the MT-ND1 (m.3460G>A), MT-ND4 (m.11778G>A) and MT-ND6 (m.14484T>C) mitochondrial genes. We found that 143B ρ0 cells devoid of mtDNA and cybrids harboring wild type mtDNA or that causing severe mitochondrial dysfunction do not produce tumors when injected in nude mice. By contrast cybrids containing mild mutant mtDNAs exhibit different tumorigenic capacities, depending on OXPHOS dysfunction.The differences in tumorigenicity correlate with an enhanced resistance to apoptosis and high levels of NOX expression. However, the final capacity of the different cybrid cell lines to generate tumors is most likely a consequence of a complex array of pro-oncogenic and anti-oncogenic factors associated with mitochondrial dysfunction.Our results demonstrate the essential role of mtDNA in tumorigenesis and explain the numerous and varied mtDNA mutations found in human tumors, most of which give rise to mild mitochondrial dysfunction.
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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.