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.
Highlights
Pancreatic ductal adenocarcinoma, the most common form of pancreatic cancer, has an overall 5-year survival rate of,5%
Pancreatic ductal adenocarcinoma is among those human tumors in which a significant overexpression of Gal-3 both on mRNA as well as on the protein level is well established [27,30]
Our own results from microarray analyses of microdissected pancreatic tumor tissues indicated that Gal-3 is expressed by the tumor cells themselves rather than by the stromal cells which typically make up the bulk of the tumor [28]
Summary
Pancreatic ductal adenocarcinoma, the most common form of pancreatic cancer, has an overall 5-year survival rate of ,5%. Galectin-3 (Gal-3), the 31 kDa member of this family, has been linked to a variety of tumors, albeit with widely differing roles [4]. Reduced Gal-3 expression in tumor tissue compared with normal tissue was reported in ovarian cancer [10], uterine adenocarcinoma [11], breast cancer [12,13] and cervical neoplasia [14]. Okada et al reported that reduced Gal-3 expression correlated with lymph node metastasis and advanced tumor stage [21], whereas two other groups identified increased expression of Gal-3 in gastric cancer, but did not find a correlation with histopathological differentiation or tumor progression [22,23]
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