C-Myc is a critical mediator of the phenotypes of Apc loss in the intestine.
The Adenomatous polyposis coli (Apc) gene is mutated in up to 80% of sporadic colorectal cancers. After Apc loss, there is deregulation of the Wnt signaling pathway and transactivation of T-cell factor/leukemia enhancing factor target genes such as C-Myc. This review focuses on recent data highlighting the importance of the C-Myc oncogene and its transcriptional targets in establishing all of the phenotypes caused by the deletion of the Apc tumor suppressor gene within the intestinal epithelium. The importance of investigating Apc and C-Myc gene function in the correct tissue context is also discussed.
Wilkins
Julie A
JA
Beatson Insitute of Cancer Research, Garscube Estate, Swithback Road, Glasgow, United Kingdom.
Sansom
Owen J
OJ
D025601:Adenomatous Polyposis Coli Protein / Q000378:metabolism; D000818:Animals; D049109:Cell Proliferation; D002471:Cell Transformation, Neoplastic / Q000235:genetics*; D017491:Genes, APC; D006801:Humans; D007413:Intestinal Mucosa / Q000378:metabolism*; D019656:Loss of Heterozygosity; D008954:Models, Biological; D010641:Phenotype; D011230:Precancerous Conditions / Q000235:genetics; D016271:Proto-Oncogene Proteins c-myc / Q000235:genetics / Q000502:physiology*
D025601:Adenomatous Polyposis Coli Protein; C489427:MYC protein, human; D016271:Proto-Oncogene Proteins c-myc