ArticleScientific reports2017
Transcriptomic analysis of mitochondrial TFAM depletion changing cell morphology and proliferation.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 53 citations in OpenAlex.
- Peptide-targeted cubosome and hexosome nanoassemblies mitigate mitochondrial dysfunction in a MitoPark model.Signal transduction and targeted therapy · 2026Article
- Mitochondrial function meets oncology: the multifaceted role of TFAM across cancer types.Apoptosis : an international journal on programmed cell death · 2026Review
- MiRNA signature analysis in LSCC gene expression profiles indicates hsa-miR-299-5p as a new tumor suppressor.Journal of applied genetics · 2026Article
- TFAM Loss Induces Oxidative Stress and Divergent Phenotypes in Glioblastoma Metabolic Subtypes.International journal of molecular sciences · 2025Article
- Prokaryotic organelle mitochondria drive tumorigenesis: "the original sin".Frontiers in oncology · 2025Review
- Decreased mitochondrial transcription factor A and mitochondrial DNA copy number promote cyclin-dependent kinase inhibitor 1A expression and reduce tumorigenic properties of colorectal cancer cells.Discover oncology · 2024Article
- The expression and clinical significance of CFAP65 in colon cancer.BMC gastroenterology · 2024Article
- Cytoplasmic DNA and AIM2 inflammasome in RA: where they come from and where they go?Frontiers in immunology · 2024Review
- A novel APA-based prognostic signature may predict the prognosis of lung adenocarcinoma in an East Asian population.iScience · 2023Article
- Role of mitochondrial alterations in human cancer progression and cancer immunity.Journal of biomedical science · 2023Review
- Gene Editing Technologies Targeting TFAM and Its Relation to Mitochondrial Diseases.Advances in experimental medicine and biology · 2023Article
- Review
- Circ_0002476 regulates cell growth, invasion, and mtDNA damage in non-small cell lung cancer by targeting miR-1182/TFAM axis.Thoracic cancer · 2022Article
- HEK293T Cells with TFAM Disruption by CRISPR-Cas9 as a Model for Mitochondrial Regulation.Life (Basel, Switzerland) · 2021Article
- Mitochondrial dysfunction, UPRCell & bioscience · 2021Review
- Mitochondrial genome and its regulator TFAM modulates head and neck tumourigenesis through intracellular metabolic reprogramming and activation of oncogenic effectors.Cell death & disease · 2021Article
- Deleterious variants in X-linked CFAP47 induce asthenoteratozoospermia and primary male infertility.American journal of human genetics · 2021Article
- A Novel Mitochondrial-Related Nuclear Gene Signature Predicts Overall Survival of Lung Adenocarcinoma Patients.Frontiers in cell and developmental biology · 2021Article
- Mitochondrial HMG-Box Containing Proteins: From Biochemical Properties to the Roles in Human Diseases.Biomolecules · 2020Review
- Role of the mitochondrial stress response in human cancer progression.Experimental biology and medicine (Maywood, N.J.) · 2020Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human mitochondrial transcription factor A (TFAM) has been implicated in promoting tumor growth and invasion. TFAM activates mitochondrial DNA (mtDNA) transcription, and affects nuclear gene expression through mitochondrial retrograde signaling. In this study, we investigated the effects of TFAM depletion on the morphology and transcriptome of MKN45 gastric cancer cells. Morphology alteration became visible at 12 h after TFAM knockdown: the proportion of growth-arrested polygonal cells versus oval-shaped cells increased, reaching a half-maximum at 24 h and a near-maximum at 36 h. TFAM knockdown upregulated four genes and downregulated six genes by more than threefold at 24 h and similarly at 48 h. Among them, the knockdown of CFAP65 (cilia and flagella associated protein 65) or PCK1 (cytoplasmic phosphoenolpyruvate carboxykinase) rescued the effects of TFAM depletion on cell morphology and proliferation. PCK1 was found to act downstream of CFAP65 in calcium-mediated retrograde signaling. Furthermore, mtDNA depletion by 2',3'-dideoxycytidine was sufficient for induction of CFAP65 and PCK1 expression and inhibition of cell proliferation, but oxidative phosphorylation blockade or mitochondrial membrane potential depolarization was not. Thus, the TFAM-mtDNA-calcium-CFAP65-PCK1 axis participates in mitochondrial retrograde signaling, affecting tumor cell differentiation and proliferation.
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