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Differential expression of prostaglandin endoperoxide H synthase-2 and formation of activated beta-catenin-LEF-1 transcription complex in mouse colonic epithelial cells contrasting in Apc

  1. Author:
    Mei, J. M.
    Hord, N. G.
    Winterstein, D. F.
    Donald, S. P.
    Phang, J. M.

  2. Author Address

    Phang JM NCI, Frederick Canc Res & Dev Ctr, Div Basic Sci, Lab Nutr & Mol Regulat Frederick, MD 21702 USA NCI, Frederick Canc Res & Dev Ctr, Div Basic Sci, Lab Nutr & Mol Regulat Frederick, MD 21702 USA NCI, Frederick Canc Res & Dev Ctr, SAIC Frederick, Intramural Res Support Program Frederick, MD 21702 USA
    1. Year: 1999
  2. Journal: Carcinogenesis
    1. 20
    2. 4
    3. Pages: 737-740
  4. Type of Article: Article
  1. Abstract:

    Mutations in Ape underlie the intestinal lesions in familial adenomatous polyposis and are found in >85% of sporadic colon cancers. They are frequently associated with overexpression of prostaglandin endoperoxide H synthase-2 (PGHS-2) in colonic adenomas. It has been suggested that Ape mutations are linked mechanistically to increased PGHS-2 expression by elevated nuclear accumulation of beta-catenin-Tcf-LEF transcription complex. In the present study, we show that PGHS-2 is differentially expressed in mouse colonic epithelial cells with distinct Ape status. Cells with a mutated Ape expressed markedly higher levels of PGHS-2 mRNA and protein and produced significantly more prostaglandin E-2 than cells with normal Ape. Using electrophoretic mobility shift assays, we demonstrate that DNA-beta-catenin-LEF-1 complex formation is differentially induced in these two cell lines in an Ape-dependent manner. Our data indicate that the differential induction of beta-catenin-LEF-1 complex correlates closely with differential expression of PGHS-2. These findings support the hypothesis that the differential expression of PGHS-2 is mediated through the proposed beta-catenin/Tcf-LEF signaling pathway. [References: 26]

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