Frequent epigenetic inactivation of SFRP genes and constitutive activation of Wnt signaling in gastric cancer View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2007-02-05

AUTHORS

M Nojima, H Suzuki, M Toyota, Y Watanabe, R Maruyama, S Sasaki, Y Sasaki, H Mita, N Nishikawa, K Yamaguchi, K Hirata, F Itoh, T Tokino, M Mori, K Imai, Y Shinomura

ABSTRACT

Activation of Wnt signaling has been implicated in gastric tumorigenesis, although mutations in APC (adenomatous polyposis coli), CTNNB1 (β-catenin) and AXIN are seen much less frequently in gastric cancer (GC) than in colorectal cancer. In the present study, we investigated the relationship between activation of Wnt signaling and changes in the expression of secreted frizzled-related protein (SFRP) family genes in GC. We frequently observed nuclear β-catenin accumulation (13/15; 87%) and detected the active form of β-catenin in most (12/16; 75%) GC cell lines. CpG methylation-dependent silencing of SFRP1, SFRP2 and SFRP5 was frequently seen among GC cell lines (SFRP1, 16/16, 100%; SFRP2, 16/16, 100%; SFRP5, 13/16, 81%) and primary GC specimens (SFRP1, 42/46, 91%; SFRP2, 44/46, 96%; SFRP5, 30/46, 65%), and treatment with the DNA methyltransferase inhibitor 5-aza-2′-deoxycytidine rapidly restored SFRP expression. Ectopic expression of SFRPs downregulated T-cell factor/lymphocyte enhancer factor transcriptional activity, suppressed cell growth and induced apoptosis in GC cells. Analysis of global expression revealed that overexpression of SFRP2 repressed Wnt target genes and induced changes in the expression of numerous genes related to proliferation, growth and apoptosis in GC cells. It thus appears that aberrant SFRP methylation is one of the major mechanisms by which Wnt signaling is activated in GC. More... »

PAGES

4699-4713

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/sj.onc.1210259

    DOI

    http://dx.doi.org/10.1038/sj.onc.1210259

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1014613226

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/17297461


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