ReviewFrontiers in oncology2017
Mitochondrial Dysfunction: A Novel Potential Driver of Epithelial-to-Mesenchymal Transition in Cancer.
Review in Frontiers in oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers, 1 of them a synthesis that pooled it.
What it found
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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.
The trial behind it
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
79 citing papers in PubMed, 1 synthesis or guideline pooled it, 181 citations in OpenAlex.
- Exposure to Heated Tobacco Products and Adverse Health Effects, a Systematic Review.International journal of environmental research and public health · 2021Pooled it
- Spatial transcriptomic profiling of ovarian clear cell carcinoma reveals heterogeneity in OXPHOS and EMT gradients.Nature communications · 2026Article
- Imbalances of mitochondrial dynamics in solid tumors.Oncogenesis · 2026Review
- Review
- Identification and validation of critical mitochondrial hub genes for prostate cancer.Oncology letters · 2026Article
- Mitochondria in the middle of inter- organellar cross talk: insights from yeast to humans.Frontiers in cell and developmental biology · 2026Review
- mTOR signaling networks: mechanistic insights and translational frontiers in disease therapeutics.Signal transduction and targeted therapy · 2025Review
- Shaping Viral Infection Outcomes via Organelle Remodeling.Annual review of virology · 2025Review
- PGC-1 alpha regulates mitochondrial biogenesis to promote silica-induced pulmonary fibrosis.Toxicology research · 2025Article
- Unveiling the powerhouse: ASCL1-driven small cell lung cancer is characterized by higher numbers of mitochondria and enhanced oxidative phosphorylation.Cancer & metabolism · 2025Article
- MtDNA copy number enrichment is associated with poor prognosis and eosinophilic morphology in clear cell renal cell carcinoma.Pathology oncology research : POR · 2025Article
- Mitochondria: a new intervention target for tumor invasion and metastasis.Molecular medicine (Cambridge, Mass.) · 2024Review
- Aging-Related Mitochondrial Dysfunction Is Associated With Fibrosis in Benign Prostatic Hyperplasia.The journals of gerontology. Series A, Biological sciences and medical sciences · 2024Article
- Metabolic alterations and mitochondrial dysfunction in human airway BEAS-2B cells exposed to vanadium pentoxide.Toxicology · 2024Article
- Identification of HSPD1 as a novel invasive biomarker associated with mitophagy in pituitary adenomas.Translational oncology · 2024Article
- Mechanisms of action of NME metastasis suppressors - a family affair.Cancer metastasis reviews · 2023Review
- Correction to: YY1 inactivated transcription co-regulator PGC-1α to promote mitochondrial dysfunction of early diabetic nephropathy-associated tubulointerstitial fibrosis.Cell biology and toxicology · 2023Article
- Adipose Mesenchymal Stem Cell-Derived Exosomes Promote the Regeneration of Corneal Endothelium Through Ameliorating Senescence.Investigative ophthalmology & visual science · 2023Article
- Metabolic factors associated with the prognosis of oligometastatic patients treated with stereotactic body radiotherapy.Cancer metastasis reviews · 2023Review
- The role of epithelial-mesenchymal transition and autophagy in pancreatic ductal adenocarcinoma invasion.Cell death & disease · 2023Review
19 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial-to-mesenchymal transition (EMT) allows epithelial cancer cells to assume mesenchymal features, endowing them with enhanced motility and invasiveness, thus enabling cancer dissemination and metastatic spread. The induction of EMT is orchestrated by EMT-inducing transcription factors that switch on the expression of "mesenchymal" genes and switch off the expression of "epithelial" genes. Mitochondrial dysfunction is a hallmark of cancer and has been associated with progression to a metastatic and drug-resistant phenotype. The mechanistic link between metastasis and mitochondrial dysfunction is gradually emerging. The discovery that mitochondrial dysfunction owing to deregulated mitophagy, depletion of the mitochondrial genome (mitochondrial DNA) or mutations in Krebs' cycle enzymes, such as succinate dehydrogenase, fumarate hydratase, and isocitrate dehydrogenase, activate the EMT gene signature has provided evidence that mitochondrial dysfunction and EMT are interconnected. In this review, we provide an overview of the current knowledge on the role of different types of mitochondrial dysfunction in inducing EMT in cancer cells. We place emphasis on recent advances in the identification of signaling components in the mito-nuclear communication network initiated by dysfunctional mitochondria that promote cellular remodeling and EMT activation in cancer cells.
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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.