Truncated APC is required for cell proliferation and DNA replication

The tumour suppressor APC is truncated in most colon cancers, which leads to the stabilization of β‐catenin and to the constitutive activation of Wnt signalling. However, it is not clear why colon cancer cells retain the truncated APC fragment. Here, we show that a decrease of APC levels achieved by...

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Bibliographic Details
Published in:International journal of cancer 2006-07, Vol.119 (1), p.74-79
Main Authors: Schneikert, Jean, Behrens, Jürgen
Format: Article
Language:English
Subjects:
APC
beta Catenin - genetics
beta Catenin - metabolism
Biological and medical sciences
Cell Cycle
Cell Proliferation
colon cancer
Colonic Neoplasms - genetics
Colonic Neoplasms - metabolism
Cyclin A - metabolism
Cyclin-Dependent Kinase Inhibitor p27 - metabolism
DNA Polymerase III - metabolism
DNA Replication
Gastroenterology. Liver. Pancreas. Abdomen
Gene Expression Regulation, Neoplastic
Genes, APC
Humans
Medical sciences
proliferation
Protein Kinases - metabolism
RNA Interference
Signal Transduction
Stomach. Duodenum. Small intestine. Colon. Rectum. Anus
Tumor Cells, Cultured
Tumors
Wnt Proteins - genetics
Wnt Proteins - metabolism
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Summary:The tumour suppressor APC is truncated in most colon cancers, which leads to the stabilization of β‐catenin and to the constitutive activation of Wnt signalling. However, it is not clear why colon cancer cells retain the truncated APC fragment. Here, we show that a decrease of APC levels achieved by RNA interference impairs cell proliferation and DNA replication, not only in 293 cells that express a wild‐type protein, but also in SW480 colon cancer cells that express exclusively a truncated APC fragment. This correlates with a reduction of the levels of cyclin A, cyclin A‐dependent kinase activity, p27kip1 and the catalytic subunit of DNA polymerase δ. Thus, our data suggest that colon cancer cells retain a truncated APC fragment because it is essential for cell proliferation. © 2006 Wiley‐Liss, Inc.
ISSN:0020-7136
1097-0215
DOI:10.1002/ijc.21826