The APC gene is mutated both in familial adenomatous polyposis (FAP) and sporadic colorectal cancers. It had been previously shown that the APC gene product interacts with beta-catenin, a key element in the Wnt-1 signaling pathway. This pathway is initiated by the growth factor Wnt-1 and ends up in the nucleus where it activates transcription factors of the Lef/Tcf family although the targets of the latter were still unknown. This has just been accomplished by the identification of the c-MYC oncogene as the relevant target of the Wnt-1/APC pathway in the development of human colorectal cancers. Indeed, under appropriate conditions (presence of growth factors, for example), c-MYC is an essential determinant of cell proliferation.
[The role of APC in colonic cancerogenesis: zeroing in on Myc]
1998-11 / vol 85 / pages 925-8
Humans; Signal Transduction; Proto-Oncogene Proteins/*metabolism; *Trans-Activators; *Zebrafish Proteins; Adenomatous Polyposis Coli Protein; Adenomatous Polyposis Coli/genetics; beta Catenin; Cytoskeletal Proteins/*metabolism; Genes, APC/*genetics/physiology; Genes, myc/*genetics/physiology; Mammary Tumor Virus, Mouse/genetics; Wnt Proteins; Wnt1 Protein