Literature DB >> 16457155

Upregulation and overexpression of DVL1, the human counterpart of the Drosophila dishevelled gene, in prostate cancer.

Kazunori Mizutani1, Shizuyo Miyamoto, Takemitsu Nagahata, Noboru Konishi, Mitsuru Emi, Masamitsu Onda.   

Abstract

AIMS AND
BACKGROUND: The Wnt/beta-catenin signaling pathway is one of the main carcinogenic mechanisms in human malignancies including prostate cancer. Recently, the DVL1 gene was identified as a middle molecule of the Wnt/beta-catenin signaling pathway. In addition, alterations of the DVL1 gene have been reported in breast and cervical cancer. The abnormality of beta-catenin in prostate cancer has been well studied, so the examination of the DVL1 gene in prostate cancer is appealing.
METHODS: We investigated DVL1 messenger RNA alterations by semiquantitative PCR (SQ-PCR) in 20 primary prostate cancers and assessed the protein expression by immunohistochemical analysis in the same samples. In addition, DVL1 and beta-catenin protein expression was evaluated with a new validated set of 20 prostate cancers.
RESULTS: SQ-PCR revealed significant overexpression of DVL1 in prostate cancer (65%). Upregulation of the DVL1 gene product in prostate cancer was confirmed by immunostaining. With SQ-PCR and immunostaining, none of the cases showed underexpression or downregulation of DVL1. In addition, the data showed correlations between DVL1 mRNA and protein expression. Interestingly, the expression level of DVL1 increased with worsening histological grade. In addition, a correlation between DVL1 expression and beta-catenin expression was confirmed.
CONCLUSIONS: DVL1 was overexpressed in prostate cancer and its overexpression might be related to prostate cancer progression through the Wnt/beta-catenin pathway.

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Year:  2005        PMID: 16457155     DOI: 10.1177/030089160509100616

Source DB:  PubMed          Journal:  Tumori        ISSN: 0300-8916


  22 in total

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10.  Sulindac inhibits canonical Wnt signaling by blocking the PDZ domain of the protein Dishevelled.

Authors:  Ho-Jin Lee; Nick X Wang; De-Li Shi; Jie J Zheng
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