ArticleOncogene2015
Metabolic reprogramming during TGFβ1-induced epithelial-to-mesenchymal transition.
Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 140 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
140 citing papers in PubMed, 220 citations in OpenAlex.
- Mesenchymal stromal/stem cells in tumour initiation, progression and therapy.Nature reviews. Cancer · 2026Review
- Cholesterol-Lowering Treatment Blocks Epithelial-Mesenchymal Transition (EMT) Associated Invasiveness and Drug Resistance in Breast and Colorectal Adenocarcinoma Models.Cancer medicine · 2026Article
- Single-cell lipidomic analysis of the epithelial-mesenchymal transition using mass spectrometry imaging.iScience · 2026Article
- Hallmarks of epithelial-mesenchymal plasticity in cancer.Molecular cancer · 2026Review
- The controversial role of metabolic reprogramming in anti-tumor therapy resistance.Discover oncology · 2026Review
- ATP synthasome contributes to efficient energy flux in malignant breast cancer.Molecular cancer · 2026Article
- TGF-β in tumor development and progression: mechanisms and therapeutics.Molecular biomedicine · 2026Review
- Unraveling the role of ChREBP in lung adenocarcinoma: Expression, regulatory networks, and potential functional impact.PloS one · 2026Article
- Advances in targeting myocardial fibrosis: integrating mechanisms and therapeutics.Frontiers in cardiovascular medicine · 2026Review
- Establishing and validating a new metabolic marker-driven prognosis signature for cutaneous melanoma.Scientific reports · 2025Article
- A preserved TGFβ cytostatic response through DLD-mediated metabolic modulation undermines anti-TGFβ therapy in gastric cancer.Nature communications · 2025Article
- Nicotinamide nucleotide transhydrogenase deficiency and genetic susceptibility to high glucose-mediated peritoneal injury in mice.Physiological reports · 2025Article
- CircZFR/YTHDF3 axis drives lymph node metastasis in cervical cancer via FASN translation.Molecular cancer · 2025Article
- Palmitic acid and palmitoylation in cancer: Understanding, insights, and challenges.Innovation (Cambridge (Mass.)) · 2025Review
- Non-canonical nuclear function of glutaminase cooperates with Wnt signaling to drive EMT during neural crest development.Nature communications · 2025Article
- Orchestrated desaturation reprogramming from stearoyl-CoA desaturase to fatty acid desaturase 2 in cancer epithelial-mesenchymal transition and metastasis.Cancer communications (London, England) · 2025Article
- Article
- Decoding chromosomal instability insights in CRC by integrating omics and patient-derived organoids.Journal of experimental & clinical cancer research : CR · 2025Article
- Crosstalk between gut microbiotas and fatty acid metabolism in colorectal cancer.Cell death discovery · 2025Review
- Role of the mInternational journal of molecular medicine · 2025Review
80 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
8 authors at 3 institutions in 1 country.
Funding
Abstract
Metastatic progression, including extravasation and micrometastatic outgrowth, is the main cause of cancer patient death. Recent studies suggest that cancer cells reprogram their metabolism to support increased proliferation through increased glycolysis and biosynthetic activities, including lipogenesis pathways. However, metabolic changes during metastatic progression, including alterations in regulatory gene expression, remain undefined. We show that transforming growth factor beta 1 (TGFβ1)-induced epithelial-to-mesenchymal transition (EMT) is accompanied by coordinately reduced enzyme expression required to convert glucose into fatty acids, and concomitant enhanced respiration. Overexpressed Snail1, a transcription factor mediating TGFβ1-induced EMT, was sufficient to suppress carbohydrate-responsive-element-binding protein (ChREBP, a master lipogenic regulator), and fatty acid synthase (FASN), its effector lipogenic gene. Stable FASN knockdown was sufficient to induce EMT, stimulate migration and extravasation in vitro. FASN silencing enhanced lung metastasis and death in vivo. These data suggest that a metabolic transition that suppresses lipogenesis and favors energy production is an essential component of TGFβ1-induced EMT and metastasis.
Indexed as
Identifiers
What OpenQuestion holds
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.