ArticleOncogene2005
High frequency of somatic mitochondrial DNA mutations in human thyroid carcinomas and complex I respiratory defect in thyroid cancer cell lines.
Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 69 citations in OpenAlex.
- The Role of Mitochondrial Genome Stability and Metabolic Plasticity in Thyroid Cancer.Biomedicines · 2025Review
- The Emerging Role of Mitochondrial Dysfunction in Thyroid Cancer: Mediating Tumor Progression, Drug Resistance, and Reshaping of the Immune Microenvironment.Biomolecules · 2025Review
- Understanding the impact of mitochondrial DNA mutations on aging and carcinogenesis (Review).International journal of molecular medicine · 2025Review
- Endocrine manifestations and long-term outcomes of patients with mitochondrial diseases.Orphanet journal of rare diseases · 2025Article
- Mitochondrial DNA common deletion in cancer: Emerging evidence and methodological challenges.Computational and structural biotechnology journal · 2025Review
- Facts, Dogmas, and Unknowns About Mitochondrial Reactive Oxygen Species in Cancer.Antioxidants (Basel, Switzerland) · 2024Review
- Toward Systems-Level Metabolic Analysis in Endocrine Disorders and Cancer.Endocrinology and metabolism (Seoul, Korea) · 2023Review
- The Interplay between Dysregulated Metabolism and Epigenetics in Cancer.Biomolecules · 2023Review
- Thyroid Cancer-Associated Mitochondrial DNA Mutation G3842A Promotes Tumorigenicity via ROS-Mediated ERK1/2 Activation.Oxidative medicine and cellular longevity · 2022Article
- High mitochondrial content is associated with breast cancer aggressiveness.Molecular and clinical oncology · 2021Article
- Four Key Steps Control Glycolytic Flux in Mammalian Cells.Cell systems · 2018Article
- Deciphering the Spectrum of Mitochondrial DNA Mutations in Hepatocellular Carcinoma Using High-Throughput Sequencing.Gene expression · 2018Article
- Article
- CRISPR/Cas9 Genome Editing of Epidermal Growth Factor Receptor Sufficiently Abolished Oncogenicity in Anaplastic Thyroid Cancer.Disease markers · 2018Article
- Mitochondrial DNA variants in colorectal carcinogenesis: Drivers or passengers?Journal of cancer research and clinical oncology · 2017Review
- Loss of p16Oncotarget · 2017Article
- Mitochondrial DNA Mutations in Grade II and III Glioma Cell Lines Are Associated with Significant Mitochondrial Dysfunction and Higher Oxidative Stress.Frontiers in physiology · 2017Article
- Interaction of Age at Diagnosis with Transcriptional Profiling in Papillary Thyroid Cancer.World journal of surgery · 2016Article
- Histone deacetylase enzyme silencing using shRNAs enhances radiosensitivity of SW579 thyroid cancer cells.Molecular medicine reports · 2016Article
- Mitochondrial variants in MT-CO2 and D-loop instability are involved in MUTYH-associated polyposis.Journal of molecular medicine (Berlin, Germany) · 2015Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Significant progress has been made to elucidate the molecular mechanisms that determine thyroid tumor development and progression. However, most investigations have mainly focused on the genetic alterations of nuclear DNA. The potential role of mitochondrial DNA (mtDNA) mutations in thyroid tumorigenesis is not well defined. In the present study, we investigated the frequency of mtDNA mutations in 24 thyroid tumor specimens (19 primary papillary thyroid carcinomas (PTC), one follicular thyroid carcinoma, and four multinodular hyperplasias) and four thyroid cancer cell lines by sequencing the entire coding regions of mitochondrial genome. Among the 19 PTC samples tested, seven (36.8%) had somatic mutations. Somatic mtDNA mutations were also detected in one of four multinodular hyperplasias examined. All the thyroid tumor cell lines carried sequence variations that change amino acid and have not been reported previously as normal sequence variants. Flow cytometry analysis of mitochondria respiratory function in the thyroid tumor cell lines revealed a severe defect in mitochondrial complex I activity. The majority of the mutations was involved in genes located in the complex I of the mitochondrial genome. The mutations were either A --> G or C --> T transitions, often resulting in a change of a moderately or highly conserved amino acid of their corresponding protein. These data suggest that mtDNA mutations may play an important role in the thyroid tumorigenesis. Given that mtDNA mutation is present in the benign multinodular hyperplasia, it might be involved in the early stage of tumor development.
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