Tumor formation by genetic mutations in the components of the Wnt signaling pathway.
The genetics of development and cancer have converged in the identification of intra- and extra-cellular signaling pathways that are aberrantly regulated in cancer, and are also central to embryonic patterning. The Wnt signaling pathway has provided an outstanding example of this. The genes for beta-catenin, APC, and Axin in the Wnt signaling pathway are often mutated in human cancers. In all such cases, the common denominator is the activation of gene transcription by beta-catenin. The resulting gene expression profile should provide a significant clue to the developmental mechanisms of cancers carrying defects in the Wnt signaling pathway. In this review, the functions of beta-catenin, APC and Axin, and the alterations of the three genes in human cancers are described.
Kikuchi
Akira
A
Department of Biochemistry, Graduate School of Biomedical Sciences, Hiroshima University. akikuchi@hiroshima-u.ac.jp
D060466:Axin Protein; D003598:Cytoskeletal Proteins / Q000235:genetics; D015972:Gene Expression Regulation, Neoplastic; D017491:Genes, APC; D006801:Humans; D009154:Mutation; D009369:Neoplasms / Q000235:genetics*; D011506:Proteins / Q000235:genetics; D011518:Proto-Oncogene Proteins / Q000235:genetics*; D012097:Repressor Proteins; D015398:Signal Transduction / Q000235:genetics; D015534:Trans-Activators / Q000235:genetics; D014158:Transcription, Genetic; D051153:Wnt Proteins; D029961:Zebrafish Proteins; D051176:beta Catenin
D060466:Axin Protein; C495270:CTNNB1 protein, human; D003598:Cytoskeletal Proteins; D011506:Proteins; D011518:Proto-Oncogene Proteins; D012097:Repressor Proteins; D015534:Trans-Activators; D051153:Wnt Proteins; D029961:Zebrafish Proteins; D051176:beta Catenin