Inhibition of EGF-dependent mitogenesis by prostaglandin E2 in Syrian hamster embryo fibroblasts

Prostaglandins, Leukotrienes, and Essential Fatty Acids
L C Hsi, T E Eling

Abstract

Lipid metabolism can play an important role in the development and progression of human cancers. We have used Syrian hamster embryo (SHE) fibroblasts as a model system to study how lipid metabolites can alter cell proliferation and apoptosis. For example, the linoleic acid metabolite 13(S)-HpODE enhances EGF-dependent growth by inhibiting de-phosphorylation of the EGFR which leads to activation of the MAP kinase pathway. In contrast, the arachidonic acid metabolite, PGE2, inhibits EGF-dependent mitogenesis and the expression of the proto-oncogenes c-myc, c-jun, and jun-B. In this study, we have investigated the mechanism by which PGE2 attenuates these responses by studying the EGF signaling cascade in SHE cells. PGE2 pretreatment caused a concentration-dependent decrease in EGF-dependent phosphorylation of MAP kinase and a corresponding inhibition of EGF-stimulated MAP kinase activity. Pretreatment of the SHE cells with PGE2 had little effect on the magnitude of EGF-dependent receptor auto-phosphorylation and the phosphorylation of GAP suggesting a down-stream target. Treatment of cells with forskolin and EGF causes similar inhibition of MAP kinase phosphorylation as observed with PGE2 and EGF. Since PGE2 elevates cAMP in these...Continue Reading

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Citations

Apr 28, 2004·The International Journal of Biochemistry & Cell Biology·Carina L BosHenri H Versteeg
Jul 8, 2009·Journal of Cellular Biochemistry·Evgeny WeinbergMiron Weinreb
Jun 20, 2017·Molecular Reproduction and Development·Agnieszka WaclawikAdam J Ziecik
Jul 11, 2001·Experimental Biology and Medicine·L LuW W Kao

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