The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
Metabolic reprogramming during TGFβ1-induced epithelial-to-mesenchymal transition
Open accessAbstract
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.
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Cites
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Self-citationATP citrate lyase is an important component of cell growth and transformation
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Understanding metabolic regulation and its influence on cell physiology
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Metabolic enzymes as oncogenes or tumor suppressors
Thompson, C. B. (2009) · New England Journal of Medicine · doi:10.1056/nejme0810213 · Cited by 213
Transforming Growth Factor β: Tumor Suppressor or Promoter? Are Host Immune Cells the Answer?
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TGF-β1–induced expression of human Mdm2 correlates with late-stage metastatic breast cancer
Araki, S., Eitel, J. A., Batuello, C. N., Bijangi-Vishehsaraei, K., Xie, X.-J., Danielpour, D., Pollok, K. E., Boothman, D. A., & Mayo, L. D. (2010) · Journal of Clinical Investigation · doi:10.1172/jci39194 · Cited by 133
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Nieto, M. A., Huang, R. Y.-J., Jackson, R. A., & Thiery, J. P. (2016) · Cell · doi:10.1016/j.cell.2016.06.028 · Cited by 4,492
Understanding the Intersections between Metabolism and Cancer Biology
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Self-citationThe multifaceted roles of fatty acid synthesis in cancer
Röhrig, F., & Schulze, A. (2016) · Nature Reviews Cancer · doi:10.1038/nrc.2016.89 · Cited by 1,651
Lipid metabolism in cancer: New perspectives and emerging mechanisms
Broadfield, L. A., Pane, A. A., Talebi, A., Swinnen, J. V., & Fendt, S.-M. (2021) · Developmental Cell · doi:10.1016/j.devcel.2021.04.013 · Cited by 758
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Metadata
- Authors
- Jiang, L., Xiao, L., Sugiura, H., Huang, X., Ali, A., Kuro-o, M., Deberardinis, R. J., & Boothman, D. A.
- Venue
- Oncogene
- Published
- 2014-10-06
- Volume
- 34
- Issue
- 30
- Pages
- 3908-3916
- ISSN
- 0950-9232 (ISSN-L)
- 1476-5594
- OpenAlex
- W1974812715
- Cited by
- 221
- References
- 7
- FWCI
- 5.35
- Type
- journal article
- Language
- en
- Open access
- green
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