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    Prostaglandin E2 stimulates Fas ligand expression via the EP1 receptor in colon cancer cells.

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    Authors
    O'Callaghan, G
    Kelly, J
    Shanahan, F
    Houston, A
    Affiliation
    Department of Medicine, University College Cork, National University of Ireland, , Clinical Science Building, Cork University Hospital, Wilton, Cork, Ireland.
    Issue Date
    2012-02-03T15:06:06Z
    MeSH
    Blotting, Western
    Cell Line, Tumor
    Coculture Techniques
    Colonic Neoplasms/*metabolism/pathology
    Dinoprostone/*pharmacology
    Enzyme-Linked Immunosorbent Assay
    Fas Ligand Protein/genetics/*metabolism
    Fluorescent Antibody Technique
    Humans
    RNA Interference
    RNA, Messenger/genetics
    Receptors, Prostaglandin E/*metabolism
    Receptors, Prostaglandin E, EP1 Subtype
    Signal Transduction
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    Citation
    Br J Cancer. 2008 Aug 5;99(3):502-12. Epub 2008 Jul 22.
    Journal
    British journal of cancer
    URI
    http://hdl.handle.net/10147/208873
    DOI
    10.1038/sj.bjc.6604490
    PubMed ID
    18648368
    Abstract
    Fas ligand (FasL/CD95L) is a member of the tumour necrosis factor superfamily that triggers apoptosis following crosslinking of the Fas receptor. Despite studies strongly implicating tumour-expressed FasL as a major inhibitor of the anti-tumour immune response, little is known about the mechanisms that regulate FasL expression in tumours. In this study, we show that the cyclooxygenase (COX) signalling pathway, and in particular prostaglandin E(2) (PGE(2)), plays a role in the upregulation of FasL expression in colon cancer. Suppression of either COX-2 or COX-1 by RNA interference in HCA-7 and HT29 colon tumour cells reduced FasL expression at both the mRNA and protein level. Conversely, stimulation with PGE(2) increased FasL expression and these cells showed increased cytotoxicity against Fas-sensitive Jurkat T cells. Prostaglandin E(2)-induced FasL expression was mediated by signalling via the EP1 receptor. Moreover, immunohistochemical analysis using serial sections of human colon adenocarcinomas revealed a strong positive correlation between COX-2 and FasL (r=0.722; P<0.0001) expression, and between EP1 receptor and FasL (r=0.740; P<0.0001) expression, in the tumour cells. Thus, these findings indicate that PGE(2) positively regulates FasL expression in colon tumour cells, adding another pro-neoplastic activity to PGE(2).
    Language
    eng
    ISSN
    1532-1827 (Electronic)
    0007-0920 (Linking)
    ae974a485f413a2113503eed53cd6c53
    10.1038/sj.bjc.6604490
    Scopus Count
    Collections
    Cork University Hospital

    entitlement

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