Prostaglandin E2 Increases Growth and Motility of Colorectal Carcinoma Cells

Hongmiao Sheng, Jinyi Shao, M. Kay Washington, Raymond N. DuBois

    Research output: Contribution to journalArticlepeer-review

    559 Scopus citations

    Abstract

    Chronic use of nonsteroidal anti-inflammatory drugs results in a significant reduction of risk and mortality from colorectal cancer in humans. All of the mechanism(s) by which nonsteroidal anti-inflammatory drugs exert their protective effects are not completely understood, but they are known to inhibit cyclooxygenase activity. The cyclooxygenase enzymes catalyze a key reaction in the conversion of arachidonic acid to prostaglandins, such as prostaglandin E2 (PGE2). Here we demonstrate that PGE 2 treatment of LS-174 human colorectal carcinoma cells leads to increased motility and changes in cell shape. The prostaglandin EP4 receptor signaling pathway appears to play a role in transducing signals which regulate these effects. PGE2 treatment results in an activation of phosphatidylinositol 3-kinase/protein kinase B pathway that is required for the PGE2-induced changes in carcinoma cell motility and colony morphology. Our results suggest that PGE2 might enhance the invasive potential of colorectal carcinoma cells via activation of major intracellular signal transduction pathways not previously reported to be regulated by prostaglandins.

    Original languageEnglish (US)
    Pages (from-to)18075-18081
    Number of pages7
    JournalJournal of Biological Chemistry
    Volume276
    Issue number21
    DOIs
    StatePublished - Jan 25 2001

    ASJC Scopus subject areas

    • Biochemistry
    • Molecular Biology
    • Cell Biology

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