ArticleThe American journal of pathology2012
Mitochondrial genome instability and ROS enhance intestinal tumorigenesis in APC(Min/+) mice.
Article in The American journal of pathology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers.
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Who cites it
93 citing papers in PubMed, 135 citations in OpenAlex.
- Colitis-associated colorectal carcinogenesis: molecular mechanisms and therapeutic potential.Molecular biomedicine · 2026Review
- Curcumin and Cancer-Related Inflammation.Nutrients · 2026Review
- The lipid transfer protein STARD7 controls intestinal tumor development in a context-dependent manner.EMBO molecular medicine · 2026Article
- Irisin as a Regulator of Brain Energy Homeostasis: Implications for Age-Related Neurodegenerative Diseases.Cells · 2026Review
- Mitochondrial function meets oncology: the multifaceted role of TFAM across cancer types.Apoptosis : an international journal on programmed cell death · 2026Review
- The Role of Mitochondrial ROS in Neoplastic Transformations, Progression and Therapeutic Targeting.Oncology research · 2026Review
- PET Imaging with [Antioxidants (Basel, Switzerland) · 2024Article
- Skeletal phenotypes and molecular mechanisms in aging mice.Zoological research · 2024Review
- Metabolism pathway-based subtyping in endometrial cancer: An integrated study by multi-omics analysis and machine learning algorithms.Molecular therapy. Nucleic acids · 2024Article
- Mitochondrial DNA replication stress triggers a pro-inflammatory endosomal pathway of nucleoid disposal.Nature cell biology · 2024Article
- ZNF281 inhibits mitochondrial biogenesis to facilitate metastasis of hepatocellular carcinoma.Cell death discovery · 2023Article
- A Th17 cell-intrinsic glutathione/mitochondrial-IL-22 axis protects against intestinal inflammation.bioRxiv : the preprint server for biology · 2023Article
- Non-lethal outcomes of engaging regulated cell death pathways in cancer.Nature cancer · 2023Review
- Long-term 1,2-dimethylhydrazine triggers pathological remodeling of colon mucosa through repression of sestrin2, nuclear factor (erythroid-derived 2)-like 2, and sirtuin4 stimulating mitochondrial stress and metabolic reprogramming.Naunyn-Schmiedeberg's archives of pharmacology · 2023Article
- Nucleolar stress: Molecular mechanisms and related human diseases.Cancer science · 2023Review
- The Role of Genetic Mutations in Mitochondrial-Driven Cancer Growth in Selected Tumors: Breast and Gynecological Malignancies.Life (Basel, Switzerland) · 2023Review
- Gene Editing Technologies Targeting TFAM and Its Relation to Mitochondrial Diseases.Advances in experimental medicine and biology · 2023Article
- TFAM loss induces nuclear actin assembly upon mDia2 malonylation to promote liver cancer metastasis.The EMBO journal · 2022Article
- A genome on shaky ground: exploring the impact of mitochondrial DNA integrity on Parkinson's disease by highlighting the use of cybrid models.Cellular and molecular life sciences : CMLS · 2022Review
- Mitochondrial genome and its regulator TFAM modulates head and neck tumourigenesis through intracellular metabolic reprogramming and activation of oncogenic effectors.Cell death & disease · 2021Article
33 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Alterations in mitochondrial oxidative phosphorylation have long been documented in tumors. Other types of mitochondrial dysfunction, including altered reactive oxygen species (ROS) production and apoptosis, also can contribute to tumorigenesis and cancer phenotypes. Furthermore, mutation and altered amounts of mitochondrial DNA (mtDNA) have been observed in cancer cells. However, how mtDNA instability per se contributes to cancer remains largely undetermined. Mitochondrial transcription factor A (TFAM) is required for expression and maintenance of mtDNA. Tfam heterozygous knock-out (Tfam(+/-)) mice show mild mtDNA depletion, but have no overt phenotypes. We show that Tfam(+/-) mouse cells and tissues not only possess less mtDNA but also increased oxidative mtDNA damage. Crossing Tfam(+/-) mice to the adenomatous polyposis coli multiple intestinal neoplasia (APC(Min/+)) mouse cancer model revealed that mtDNA instability increases tumor number and growth in the small intestine. This was not a result of enhancement of Wnt/β-catenin signaling, but rather appears to involve a propensity for increased mitochondrial ROS production. Direct involvement of mitochondrial ROS in intestinal tumorigenesis was shown by crossing APC(Min/+) mice to those that have catalase targeted to mitochondria, which resulted in a significant reduction in tumorigenesis in the colon. Thus, mitochondrial genome instability and ROS enhance intestinal tumorigenesis and Tfam(+/-) mice are a relevant model to address the role of mtDNA instability in disease states in which mitochondrial dysfunction is implicated, such as cancer, neurodegeneration, and aging.
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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.