Cytoskeleton out of the cupboard: colon cancer and cytoskeletal changes induced by loss of APC.
Mutation of APC (adenomatous polyposis coli) is a common factor in most colorectal cancers. APC has many functions, the most prominent is its capacity to regulate beta-catenin-mediated gene transcription in response to Wnt signalling. Loss of APC leads to deregulated beta-catenin and this is intimately linked with tumour formation. However, recent evidence indicates that the interaction of APC with the cytoskeleton might also contribute to tumour initiation and progression. How does APC interact with the cytoskeleton and how could this play a part in colorectal tumorigenesis?
Näthke
Inke
I
Division of Cell & Developmental Biology, University of Dundee, Dow Street, Dundee DD1 5EH, Scotland, UK. inke@lifesci.dundee.ac.uk
D025601:Adenomatous Polyposis Coli Protein / Q000235:genetics / Q000378:metabolism*; D017209:Apoptosis; D002454:Cell Differentiation; D002465:Cell Movement; D049109:Cell Proliferation; D003110:Colonic Neoplasms / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D003598:Cytoskeletal Proteins / Q000378:metabolism; D003599:Cytoskeleton / Q000378:metabolism*; D015972:Gene Expression Regulation, Neoplastic; D017491:Genes, APC; D006801:Humans; D007413:Intestinal Mucosa / Q000378:metabolism; D009154:Mutation; D015398:Signal Transduction; D051176:beta Catenin / Q000378:metabolism
D025601:Adenomatous Polyposis Coli Protein; D003598:Cytoskeletal Proteins; D051176:beta Catenin