ArticleActa pharmacologica Sinica2010
The epoxyeicosatrienoic acid-stimulated phosphorylation of EGF-R involves the activation of metalloproteinases and the release of HB-EGF in cancer cells.
Article in Acta pharmacologica Sinica, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- Metabolic Targets in CRC: The Emerging Role of Cytochrome P450 Inhibitors.Current pharmaceutical design · 2025Review
- Epidermal growth factor receptor transactivation is involved in the induction of human hepatoma SMMC7721 cell proliferation by insufficient radiofrequency ablation.Oncology letters · 2017Article
- Addition of DHA Synergistically Enhances the Efficacy of Regorafenib for Kidney Cancer Therapy.Molecular cancer therapeutics · 2016Article
- Epoxyeicosatrienoic acids protect rat hearts against tumor necrosis factor-α-induced injury.Journal of lipid research · 2012Article
- Epoxides and soluble epoxide hydrolase in cardiovascular physiology.Physiological reviews · 2012Review
- Epoxyeicosatrienoic acids: a double-edged sword in cardiovascular diseases and cancer.The Journal of clinical investigation · 2012Article
- EET signaling in cancer.Cancer metastasis reviews · 2011Review
- Cytochrome P450 epoxygenase CYP2J2 attenuates nephropathy in streptozotocin-induced diabetic mice.Prostaglandins & other lipid mediators · 2011Article
- Inhibition of carcinoma cell motility by epoxyeicosatrienoic acid (EET) antagonists.Cancer science · 2010Article
- Clinical significance of EPHX2 deregulation in prostate cancer.Asian journal of andrologyArticle
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
aimTo test the hypothesis that the epoxyeicosatrienoic acid (EET)-induced transactivation of EGF-R depends on the activation of metalloproteinases and the subsequent release of HB-EGF in cancer cells.
methodsExogenous 14,15-EET were added to four human-derived cancer cell lines Tca-8113, A549, HepG2, and MDA-MB-231, or these same cell lines were transfected with a mutant CYP epoxygenase (CYP102 F87V, an active 14,15-epoxygenase). The effects of elevated EET levels on the phosphorylation of tyrosine residues in the EGF receptor and on ERK1/2 activation were then assessed.
resultsBoth the addition of 14,15-EET and the transfection of cells with CYP102 F87V markedly increased the phosphorylation of the tyrosine residues of EGF-R and ERK1/2, an effect that was blocked by a selective EGF-R tyrosine kinase inhibitor (tyrphostin AG1478), a broad-spectrum metalloproteinase inhibitor (1,10-phenanthroline), and an inhibitor of HB-EGF release (CRM197) in Tca-8113 cells. In addition, AG1478, 1,10-phenanthroline, and CRM197 also inhibited the tyrosine phosphorylation of EGF-R and ERK1/2 that was induced by 14,15-EET in the A549, HepG2, and MDA-MB-231 cell lines.
conclusionThese results suggest that the EET-induced transactivation of EGF-R depends on activation of metalloproteinases and the subsequent release of HB-EGF in cancer cell lines.
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