1Nikolaus-Fiebiger-Center for Molecular Medicine, University Erlangen-Nürnberg, Erlangen, Germany and 2Clinic for Abdominal, Endocrine and Thoracic Surgery, Klinikum Nürnberg, Nürnberg, Germany.
Wnt signaling has been identified as one of the key signaling pathways in
cancer, regulating cell growth, motility and differentiation. Because of its widespread activation in diverse human tumor diseases, the Wnt pathway has gained considerable and growing interest in
tumor research over recent years. Evidence that altered Wnt signaling is important for human
tumor development came from three major findings: (i) the tumor suppressor adenomatous polyposis
coli (APC) binds to the Wnt pathway component β-catenin and is involved in its degradation,
(ii) mutations of APC in colon tumors lead to stabilization of the β-catenin protein and (iii) tumor-associated mutations of β-catenin in colorectal cancer as well as in other tumor types lead to its stabilisation, qualifying β-catenin as a proto-oncogene. Here we will describe the biochemical interactions which shape the Wnt pathway and focus on its role in tumorigenesis.