Premium
Axin, an inhibitor of the Wnt signalling pathway, interacts with β‐catenin, GSK‐3β and APC and reduces the β‐catenin level
Author(s) -
Nakamura Tsutomu,
Hamada Fumihiko,
Ishidate Takao,
Anai Kenichi,
Kawahara Kohichi,
Toyoshima Kumao,
Akiyama Tetsu
Publication year - 1998
Publication title -
genes to cells
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.912
H-Index - 115
eISSN - 1365-2443
pISSN - 1356-9597
DOI - 10.1046/j.1365-2443.1998.00198.x
Subject(s) - wnt signaling pathway , adenomatous polyposis coli , catenin , gsk 3 , biology , beta catenin , microbiology and biotechnology , effector , hedgehog signaling pathway , carcinogenesis , axin2 , cancer research , glycogen synthase , kinase , signal transduction , colorectal cancer , phosphorylation , genetics , cancer
Background: The Wnt/Wingless signalling pathway plays an important role in both embryonic development and tumorigenesis. β‐Catenin and Axin are positive and negative effectors of the Wnt signalling pathway, respectively. Results: We found that Axin interacts with β‐catenin and glycogen synthase kinase‐3β (GSK‐3β). Furthermore, the regulation of the G‐protein signalling (RGS) domain of Axin is associated with the colorectal tumour suppressor adenomatous polyposis coli (APC). Overexpression of Axin in the human colorectal cancer cell line SW480 induced a drastic reduction in the level of β‐catenin. Interaction with β‐catenin and GSK‐3β was required for the Axin‐mediated β‐catenin reduction. Conclusion: Axin interacts with β‐catenin, GSK‐3β and APC, and negatively regulates the Wnt signalling pathway, presumably by regulating the level of β‐catenin.