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

Abstract

Syndecan‐1 belongs to the syndecan family of cell surface transmembrane heparan‐sulfate proteoglycans, which participate in cell proliferation, cell migration and cell‐matrix interactions. Decreased expression of syndecan‐1 has been observed in some gastrointestinal malignancies, and it is thought that high levels of syndecan‐1 correlate with the maintenance of epithelial morphology and inhibition of invasiveness. In our study, we characterized the 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 comparison with both chronic pancreatitis (2.4‐fold increase, p < 0.01) and normal pancreatic samples (10.6‐fold increase, p < 0.01). There was no difference in syndecan‐1 mRNA expression between early and advanced tumors. By in situ hybridization and immunohistochemistry, syndecan‐1 expression was evident at relatively low levels in the ductal cells and less frequently in acinar cells of the normal pancreas. In chronic pancreatitis, syndecan‐1 was present at low to moderate levels in areas with atrophic acinar cells and ductular complexes. In contrast, in pancreatic cancer tissues, syndecan‐1 was present at moderate to high levels in the majority of the cancer cells within the tumor mass and also in metastatic lesions of pancreatic tumors. Syndecan‐1 mRNA levels in other gastrointestinal malignancies (esophageal, gastric, colon and liver cancers) were not significantly different from the levels observed in the corresponding normal samples. Together, our findings suggest that syndecan‐1 expression by pancreatic cancer cells may be of importance in the pathobiology of this disorder and that its role in pancreatic cancer seems to be different from that in other gastrointestinal malignancies. Int. J. Cancer 88:12–20, 2000. © 2000 Wiley‐Liss, Inc.

Shedding; towards a new paradigm of syndecan function in cancer

“…Consistent with this, overexpression of syndecan-1 has bee shown to induce approximately a twofold increase in the proliferation of endometrial cancer cells (26). Syndecan-1 mRNA levels are up-regulated in pancreatic cancer in association with accelerated tumor growth, as determined by in situ hybridization and immunohistochemistry (27).…”

Fiber-chimeric adenoviruses expressing fibers from serotype 16 and 50 improve gene transfer to human pancreatic adenocarcinoma

“…41 Overexpression of integrins and the HSPGs syndecan-1 and glypican-1 on pancreatic cancer will mediate transduction by Ad5 and will thus lower the effect of retargeting strategies. 7,42,43 However, because these proteins will also have an important function in vivo the targeting seen in these slices will reflect the efficacy of retargeting of this vector in patients.…”

Syndecan as a Messenger to Link Diabetes and Cancer

“…It has been found that syndecan-1 promotes the metastases in lung squamous carcinoma cells (Hirabayashi et al, 1998). The overexpression of syndecan-1 expression has been observed in various cancer such as pancreatic (Conejo et al, 2000), gastric (Wiksten et al, 2001) and breast (Stanley et al, 1999;Barbareschi et al, 2003;Burbach et al, 2003) carcinomas.…”