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Pancreas. 2008 Nov;37(4):399-404. doi: 10.1097/MPA.0b013e31817f76f7.

Expression of kallikrein 7 diminishes pancreatic cancer cell adhesion to vitronectin and enhances urokinase-type plasminogen activator receptor shedding.

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Department of Pathology, Winthrop P. Rockefeller Cancer Institute, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA.



To examine the effects of kallikrein 7 (KLK7) expression in pancreatic cancer cells on cell adhesion to extracellular matrix proteins.


Kallikrein 7 was overexpressed in the pancreatic cancer cell line BxPC-3, and in vitro cell adhesion assays were performed to determine alterations in cell adhesion to collagen I, fibronectin, and vitronectin compared with vector-transfected cells. Changes in cell surface expression of alphavbeta3 integrin were examined by flow cytometry, and the release of soluble urokinase-type plasminogen activator receptor (uPAR) was monitored by Western blot analysis.


The expression of KLK7 in BxPC-3 cells led to reduced adhesion to vitronectin but not collagen I or fibronectin. Loss of cell adhesion to vitronectin was not caused by changes in the level of alphavbeta3 integrin cell surface expression; however, a significant increase in the amount of uPAR shed was observed in KLK7-expressing cells compared with vector-transfected control cells.


The aberrant expression of KLK7 in pancreatic cancer cells leads to a reduction in cell adhesion to vitronectin that may result from the cleavage of uPAR from the cell surface. Kallikrein 7 expression, therefore, may play an important role in the dissemination of tumor cells through the production of soluble uPAR in pancreatic cancer and perhaps other human malignancies.

[Indexed for MEDLINE]

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