comprehensive analysis of cellular galectin-3 reveals no consistent oncogenic function in pancreatic cancer cells综合分析细胞galectin-3在胰腺癌细胞显示不一致的致癌作用.pdf

Comprehensive Analysis of Cellular Galectin-3 Reveals No Consistent Oncogenic Function in Pancreatic Cancer Cells . . Alexander Hann* , Anja Gruner , Ying Chen, Thomas M. Gress , Malte Buchholz Department of Gastroenterology, Endocrinology and Metabolism, Philipps-University of Marburg, Marburg, Germany 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