期刊
EXPERIMENTAL CELL RESEARCH
卷 317, 期 6, 页码 838-848出版社
ELSEVIER INC
DOI: 10.1016/j.yexcr.2010.12.025
关键词
Soluble E-cadherin; Apoptosis; Cancer; Epidermal growth factor receptor (EGFR); Phosphoinositide-3 kinase (PI3K); Erk1/2
资金
- NIH [DK 56216, F31-GM068985]
- American Heart Association [10SDG4170012]
High levels of the soluble form of E-cadherin can be found in the serum of cancer patients and are associated with poor prognosis. Despite the possible predictive value of soluble E-cadherin, little is understood concerning its patho-physiological consequences in tumor progression. In this study, we show that soluble E-cadherin facilitates cell survival via functional interaction with cellular E-cadherin. Exposure of cells to a recombinant form of soluble E-cadherin, at a concentration found in cancer patient's serum, prevents apoptosis due to serum/growth factor withdrawal, and inhibits epithelial lumen formation, a process that requires apoptosis. Further, soluble E-cadherin-mediated cell survival involves activation of the epidermal growth factor receptor (EGFR) and EGFR-mediated activation of both phosphoinositide-3 kinase (PI3K)/AKT and ERK1/2 signaling pathways. These results are evidence of a complex functional interplay between EGER and E-cadherin and also suggest that the presence of soluble E-cadherin in cancer patients' sera might have relevance to cell survival and tumor progression. (C) 2011 Elsevier Inc. All rights reserved.
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