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PLoS One. 2011;6(6):e20859. doi: 10.1371/journal.pone.0020859. Epub 2011 Jun 16.

Comprehensive analysis of cellular galectin-3 reveals no consistent oncogenic function in pancreatic cancer cells.

Author information

1
Department of Gastroenterology, Endocrinology and Metabolism, Philipps-University of Marburg, Marburg, Germany. hanna@med.uni-marburg.de

Abstract

Galectin-3 (Gal-3), a 31 kDa member of the family of beta-galactoside-binding proteins, has been implicated in the progression of different human cancers. However, the proposed roles differ widely, ranging from tumor-promoting cellular functions and negative impact on patient prognosis to tumor-suppressive properties and positive prognostic impact. We and others have previously identified Gal-3 as overexpressed in pancreatic cancer as compared to chronic pancreatitis and normal pancreatic tissue. The purpose of this study was thus the comprehensive analysis of putative cellular functions of Gal-3 by transient as well as stable silencing or overexpression of Gal-3 in a panel of 6 well-established pancreatic cancer cell lines. Our results confirm that galectin-3 is upregulated at the mRNA level in pancreatic cancer and strongly expressed in the majority of pancreatic cancer cell lines. In individual cell lines, transient knockdown of Gal-3 expression resulted in moderate inhibitory effects on proliferation, migration or anchorage-independent growth of the cells, but these effects were not consistent across the spectrum of analyzed cell lines. Moreover, functional effects of the modulation of Gal-3 expression were not observed in stable knockdown or overexpression approaches in vitro and did not alter the growth characteristics of nude mouse xenograft tumors in vivo. Our data thus do not support a direct functional role of Gal-3 in the malignant transformation of pancreatic epithelial cells, although paracrine or systemic effects of Gal-3 expression are not excluded.

PMID:
21698183
PMCID:
PMC3116838
DOI:
10.1371/journal.pone.0020859
[Indexed for MEDLINE]
Free PMC Article

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