Pancreatic Cancer
Sulf1 mRNA expression in pancreatic cancer differed from ovarian and liver cancer. Only 50% of pancreatic cancer cell lines tested exhibited a significant decrease in Sulf1. Further, in situ hybridization demonstrated that Sulf1 mRNA expression was not uniformly absent in pancreatic cancer tissue. In fact, Sulf1 was present weakly in normal acinar cells, but present at high levels in the endothelium and malignant cells in pancreatic cancer tissue (Li, Kleeff et al. 2005). This indicates that downregulation of Sulf1 is not a ubiquitous process in carcinogenesis. Nevertheless, endogenous expression of Sulf1 in a Sulf1-negative pancreatic cancer cell line, Panc-1, inhibited FGF-2 signaling, but did not affect HB-EGF, EGF, or insulin-like growth factor-1 (IGF-1) signaling, indicating cell specific effects. In further contrast to ovarian cancer and HCC, Hsulf-1 expressing Panc-1 cells were more resistant to gemcitabine, suggesting Hsulf-1 over-expression might confer increased chemoresistance, and therefore a growth advantage, to pancreatic cancer cells. In further reports Sulf1 displays a complicated expression pattern in pancreatic cancer that is more than merely up or downregulation. For instance, primary pancreatic cancer show higher sulfated HSPGs indicating a lack of Sulf1, but upon metastasis sulfation of HSPGs is reduced. Corroborating patient data were mouse tumor in vivo studies of Sulf1 overexpressing Panc-1 cells showing decreased growth, but increased local invasiveness.
Read more about this topic: SULF1, Role in Cancer
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