Syndecan-1 expression is up-regulated in pancreatic but not in other gastrointestinal cancers

Syndecan-1 belongs to the syndecan family of cell surface transmembrane hep aran-sulfate proteoglycans, which participate in cell proliferation, cell m igration and cell-matrix interactions. Decreased expression of syndecan-1 h as been observed in some gastrointestinal malignancies, and it is thought t hat high levels of syndecan-1 correlate with the maintenance of epithelial morphology and inhibition of invasiveness. In our study, we characterized t he expression of syndecan-1 in normal, chronic pancreatitis and primary and metastatic human pancreatic cancer tissues, in cultured pancreatic cancer cell lines and in esophageal, gastric, colon, and liver cancers. Pancreatic cancer cell lines expressed syndecan-1 mRNA and protein at variable levels . In addition, these cells also released syndecan-1 into the culture medium . Pancreatic cancer tissues markedly over-expressed syndecan-1 mRNA in comp arison with both chronic pancreatitis (2.4-fold increase, p < 0.01) and nor mal pancreatic samples(10.6-fold increase, p < 0.01). There was no differen ce in syndecan-1 mRNA expression between early and advanced tumors. By in s itu hybridization and immunohistochemistry, syndecan-1 expression was evide nt at relatively low levels in the ductal cells and less frequently in acin ar cells of the normal pancreas. In chronic pancreatitis, syndecan-1 was pr esent at low to moderate levels in areas with atrophic acinar cells and duc tular complexes. In contrast, in pancreatic cancer tissues, syndecan-1 was present: at moderate to high levels in the majority of the cancer cells wit hin the tumor mass and also in metastatic lesions of pancreatic tumors. Syn decan-1 mRNA levels in other gastrointestinal malignancies (esophageal, gas tric, colon and liver cancers) were not significantly different from the le vels observed in the corresponding normal samples. Together, our findings s uggest that syndecan-1 expression by pancreatic cancer cells may be of impo rtance in the pathobiology of this disorder and that its role in pancreatic cancer seems to be different from that in other gastrointestinal malignanc ies. (C) 2000 Wiley-Liss, Inc.