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JHC exPRESS: First Published August 22, 2005. doi:10.1369/jhc.5A6626.2005
Copyright © Histochemical Society, Inc.

A more recent version of this article appeared on February 1, 2006.
Originally published as JHC exPRESS on August 8, 2005.
doi:10.1369/jhc.5A6626.2005
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Aberrant Gata-3 Expression in Human Pancreatic Cancer

Antanas Gulbinas 1, Pascal O. Berberat 1, Zilvinas Dambrauskas 1, Thomas Giese 1, Nathalia Giese 1, Frank Autschbach 1, Joerg Kleeff 1, Stefan Meuer 1, Markus W. Büchler 1 and Helmut Friess 1*

1 Department of General Surgery (AG,POB,ZD,NG,JK,MWB,HF), Institute of Immunology (POB,TG,SM) and Department of Pathology (FA), University of Heidelberg, Heidelberg, Germany

* To whom correspondence should be addressed. E-mail: helmut_friess{at}med.uni-heidelberg.de.

Submitted on January 18, 2005
Accepted on 11 July 2005


  Abstract
Gata-3 has been shown to specifically alter its expression patterns in different types of cancers. Recent evidence suggests that an interference of Gata-3 exists in the TGF-{beta} signaling pathway. To determine the role of Gata-3 in pancreatic cancer, pancreatic cancer samples were analyzed in comparison to normal pancreatic tissues. Furthermore, four different pancreatic cancer cell lines with different alterations of the TGF-{beta} pathway were studied. To evaluate if a potential relationship with TGF-{beta} signaling pathway exists, we correlated mRNA expression levels with the expression of TGF-{beta}s, TGF-{beta} receptors and smad-3. Finally, we analyzed the influence of TGF-{beta} on Gata-3 expression in vitro. All pancreatic cancer samples demonstrated a marked overexpression of Gata-3 mRNA and protein. Immunohistochemical staining revealed strong and persistent cytoplasmatic Gata-3 immunoreactivity in cancer cells. In an electrophoretic mobility shift assay, a disturbed nuclear translocation was confirmed. The expression of Gata-3 showed a significant correlation with the expression of TGF-{beta}s, TGF-{beta} receptors and Smad-3. TGF-{beta} responsive cell lines showed a down-regulation of Gata-3 mRNA upon TGF-{beta} exposure, whereas in TGF-{beta} unresponsive cell lines, Gata-3 mRNA expression persisted on high levels. Furthermore, strong specific up-regulation of Gata-3, impaired nuclear translocation and its cooperative action with the TGF-{beta} pathway, suggesting that Gata-3 plays a central role in human pancreatic cancer.

Key Words: Gata-3, TGF-{beta}, pancreas, pancreatic cancer


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