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  • Title: Prostaglandin E2 enhances mitogen-activated protein kinase/Erk pathway in human cholangiocarcinoma cells: involvement of EP1 receptor, calcium and EGF receptors signaling.
    Author: Zhang L, Jiang L, Sun Q, Peng T, Lou K, Liu N, Leng J.
    Journal: Mol Cell Biochem; 2007 Nov; 305(1-2):19-26. PubMed ID: 17551669.
    Abstract:
    COX-2-derived PGE2 has been implicated in the development of various types of cancers. However, the exact mechanism of PGE2-induced cancer cell proliferation and survival is still unclear. In the current study, the mechanism underlying PGE2-enhanced Erk phosphorylation in human cholangiocarcinoma cells was determined. The intracellular concentration of calcium in three cholangiocarcinoma cell lines was measured using a laser confocal scanning microscope and the expression levels of Erk and EGFR phosphorylation were determined by Western blot analyses. The activation of EP1 receptors involved in PGE2-stimulated Erk activation and increasing the intracellular concentration of calcium was elucidated using selective EP1 receptor subtype antagonists and agonist. The intracellular calcium chelator, BAPTA-AM, was shown to block PGE2-induced Erk and EGFR phosphorylation. PGE2-induced Erk phosphorylation was abrogated by pretreatment with the EGF receptor kinase inhibitor, AG1478. Our findings suggest that in human cholangiocarcinoma cells, PGE2-enhanced phosphorylation of Erk is, at least in part, mediated through EP1 receptors and EGFR phosphorylation induced by increases in the intracellular concentration of calcium.
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