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SMAF‐1 Inhibits the APC/β‐Catenin Pathway and Shows Properties Similar to Those of the Tumor Suppressor Protein APC
Author(s) -
Karaguni IoannaMaria,
Gourzoulidou Eleni,
Carpintero Mercedes,
Langerak Anette,
KleinHitpaß Ludger,
Möröy Tarik,
Winde Günther,
Waldmann Herbert,
Müller Oliver
Publication year - 2004
Publication title -
chembiochem
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.05
H-Index - 126
eISSN - 1439-7633
pISSN - 1439-4227
DOI - 10.1002/cbic.200400078
Subject(s) - adenomatous polyposis coli , sulindac , suppressor , catenin , familial adenomatous polyposis , chemistry , cancer research , microbiology and biotechnology , p53 protein , apoptosis , gene , biology , biochemistry , colorectal cancer , wnt signaling pathway , cancer , genetics , pharmacology , nonsteroidal
The NSAID Sulindac inhibits the proliferation of cells with mutations in the tumor‐suppressor gene APC (Adenomatous Polyposis coli). We introduce here a Sulindac homologue, SMAF‐1 and show that it inhibits the proliferation of cells with activated APC/β‐catenin pathway and is able to induce apoptosis. SMAF‐1 incubated cells show a decreased β‐catenin level accompanied by a decrease in β‐catenin‐induced gene expression. Our results support the hypothesis that SMAF‐1 and NSAIDs like Sulindac execute major functions of the APC protein.