ArticleScientific reports2018
Mitochondrial transcription factor A (TFAM) shapes metabolic and invasion gene signatures in melanoma.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
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The trial behind it
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Who cites it
33 citing papers in PubMed, 55 citations in OpenAlex.
- Macrophage anti-bacterial activity is controlled by adenylate kinase 4-mediated mitochondrial DNA synthesis.The Journal of experimental medicine · 2026Article
- Multi-omics profiling identifies ectopic olfactory receptors as putative drivers of tumor progression and prognostic indicators in clear cell renal cell carcinoma.Clinical and experimental medicine · 2026Article
- Mitochondrial function meets oncology: the multifaceted role of TFAM across cancer types.Apoptosis : an international journal on programmed cell death · 2026Review
- TFAM Loss Induces Oxidative Stress and Divergent Phenotypes in Glioblastoma Metabolic Subtypes.International journal of molecular sciences · 2025Article
- Therapeutic Potential of Glutaminase Inhibition Targeting Metabolic Adaptations in Resistant Melanomas to Targeted Therapy.International journal of molecular sciences · 2025Article
- Expression of mitochondrial transcription factor A in granulosa cells: implications for oocyte maturation and in vitro fertilization outcomes.Journal of assisted reproduction and genetics · 2024Article
- Integrative analysis identifies oxidative stress biomarkers in non-alcoholic fatty liver disease via machine learning and weighted gene co-expression network analysis.Frontiers in immunology · 2024Article
- Integrating mitoepigenetics into research in mood disorders: a state-of-the-art review.Frontiers in physiology · 2024Review
- Mitochondrial DNA-targeted therapy: A novel approach to combat cancer.Cell insight · 2023Review
- Article
- Gene Editing Technologies Targeting TFAM and Its Relation to Mitochondrial Diseases.Advances in experimental medicine and biology · 2023Article
- Isoforms of the transcriptional cofactor SIN3 differentially regulate genes necessary for energy metabolism and cell survival.Biochimica et biophysica acta. Molecular cell research · 2022Article
- Induced Zinc Loss Produces Heterogenous Biological Responses in Melanoma Cells.International journal of molecular sciences · 2022Article
- Mitochondrial Genetic and Epigenetic Regulations in Cancer: Therapeutic Potential.International journal of molecular sciences · 2022Review
- TFAM loss induces nuclear actin assembly upon mDia2 malonylation to promote liver cancer metastasis.The EMBO journal · 2022Article
- Benchmarking the Effectiveness and Accuracy of Multiple Mitochondrial DNA Variant Callers: Practical Implications for Clinical Application.Frontiers in genetics · 2022Article
- Mitochondrial Epigenetics Regulating Inflammation in Cancer and Aging.Frontiers in cell and developmental biology · 2022Review
- HEK293T Cells with TFAM Disruption by CRISPR-Cas9 as a Model for Mitochondrial Regulation.Life (Basel, Switzerland) · 2021Article
- Mitochondrial genome and its regulator TFAM modulates head and neck tumourigenesis through intracellular metabolic reprogramming and activation of oncogenic effectors.Cell death & disease · 2021Article
- Mitochondrial transcription factor A plays opposite roles in the initiation and progression of colitis-associated cancer.Cancer communications (London, England) · 2021Article
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 3 countries.
Funding
Abstract
Mitochondria are central key players in cell metabolism, and mitochondrial DNA (mtDNA) instability has been linked to metabolic changes that contribute to tumorigenesis and to increased expression of pro-tumorigenic genes. Here, we use melanoma cell lines and metastatic melanoma tumors to evaluate the effect of mtDNA alterations and the expression of the mtDNA packaging factor, TFAM, on energetic metabolism and pro-tumorigenic nuclear gene expression changes. We report a positive correlation between mtDNA copy number, glucose consumption, and ATP production in melanoma cell lines. Gene expression analysis reveals a down-regulation of glycolytic enzymes in cell lines and an up-regulation of amino acid metabolism enzymes in melanoma tumors, suggesting that TFAM may shift melanoma fuel utilization from glycolysis towards amino acid metabolism, especially glutamine. Indeed, proliferation assays reveal that TFAM-down melanoma cell lines display a growth arrest in glutamine-free media, emphasizing that these cells rely more on glutamine metabolism than glycolysis. Finally, our data indicate that TFAM correlates to VEGF expression and may contribute to tumorigenesis by triggering a more invasive gene expression signature. Our findings contribute to the understanding of how TFAM affects melanoma cell metabolism, and they provide new insight into the mechanisms by which TFAM and mtDNA copy number influence melanoma tumorigenesis.
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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.