Journal
PATHOLOGY RESEARCH AND PRACTICE
Volume 210, Issue 10, Pages 668-674Publisher
ELSEVIER GMBH
DOI: 10.1016/j.prp.2014.06.016
Keywords
Colorectal cancer; Liver metastasis; Integrin; Fak; CD98
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Funding
- Research Institute of McGill University Health Center
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CD98-mediated beta 1 and beta 3 integrins activation can induce Fak phosphorylation which eventually promotes cell survival, proliferation, and migration. We evaluated the expression of CD98, integrin beta 1, integrin beta 3 and Fak in 45 cases of matched colorectal cancer (CRC) and liver metastases as well as 35 cases of CRC without liver metastases. There was a gradual increase of the expression of CD98, integrin beta 1, integrin beta 3 and Fak as tumor progressed from normal colon to carcinoma to budding tumor cells at the invasive front and to liver metastases. The expression of CD98 and integrin beta 1 in CRC with liver metastases was significantly higher than that in CRC without liver metastases. Furthermore, for those liver metastases with desmoplastic growth pattern, expression of CD98, integrin beta 1, integrin beta 3 and Fak at the metastases center was as strong as that at the metastases periphery. For those liver metastases with pushing or replacement growth patterns, more intense expression of these markers was found at the metastases center than the periphery. Overexpression of CD98, integrin beta 1, integrin beta 3 and Fak is associated with the progression and liver metastases of CRC. Overexpression of these markers in liver metastases requires direct contact between tumor cells and the stroma. (C) 2014 Elsevier GmbH. All rights reserved.
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