IMR Press / FBL / Volume 10 / Issue 2 / DOI: 10.2741/1605

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.

Involvement of adenomatous polyposis coli in colorectal tumorigenesis
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1 Department of Anatomy and Cell Biology and UF Shands Cancer Center, University of Florida, Gainesville, FL 32610-0232, USA
Front. Biosci. (Landmark Ed) 2005, 10(2), 1118–1134;
Published: 1 May 2005

Colorectal cancer arises after a series of mutations in various tumor suppressor and proto-oncogenes, each of which is accompanied by specific alterations and pathological conditions. Recent advances have contributed a great deal of understanding of the molecular basis of events that lead to colorectal tumorigenesis. Mutation in the adenomatous polyposis coli (APC) gene is considered to be one of the earliest events in the colon cancer development. The familial adenomatous polyposis (FAP) and hereditary nonpolyposis colorectal cancer (HNPCC) are the most commonly inherited colorectal cancers. FAP and HNPCC develop due to mutations in APC and DNA mismatch repair (MMR) genes, respectively. APC is known to regulate the levels of beta-catenin, an important mediator of cell-cell adhesion and transcriptional regulator. Mutations in APC gene are also linked with chromosomal instability in colon cancer cells. The role of APC is also implicated in cell migration, cell-cell adhesion, cell cycle control, and apoptosis. This article summarizes the structure-function studies and the role of APC mutations in colon cancer development.

Adenomatous polyposis coli
Beta-catenin levels
Cell cycle regulation
Cell migration and adhesion
Colorectal cancer
Chromosomal instability
Familial adenomatous polyposis
Mutator cluster region
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