Year: 2016
Type: article
Abstract: Adenomatous polyposis coli (APC) is widely accepted as a tumor suppressor gene highly mutated in colorectal cancers (CRC). Mutation and inactivation of this gene is a key and early event almost uniquely observed in colorectal tumorigenesis. Alterations in the APC gene generate truncated gene products, leading to activation of the Wnt signaling pathway and deregulation of multiple other cellular processes. It has been a mystery why most patients with CRC retain a truncated APC protein, but accumulating evidence suggest that these C terminally truncated APC proteins may have gain of function properties beyond the well-established loss of tumor suppressive function. Here, we will review the evidence for both the loss of function and the gain of function of APC truncations and how together they contribute to CRC initiation and progression.
DOI: 10.1093/jnci/djw332
Authors: Lu Zhang, Jerry W. Shay
Institution: The University of Texas Southwestern Medical Center
Language: English
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: bronze
Awards: Cell Biology Research Improvements and Renovations, Development of Therapeutics Targeting Truncated Adenomatous Polyposis Coli (APC) as a Novel Prevention and Intervention Strategy for Colorectal Cancer, Development of Therapeutics Targeting Truncated Adenomatous Polyposis Coli (APC) as a Novel Prevention and Intervention Strategy for Colorectal Cancer
OpenAlex ID: W2605230952