Insulin-like growth factor-I (IGF-I) is upregulated in human pancreatic cancer tissues but is not expressed in surrounding non-cancerous tissues. Serum level of IGF-I is elevated in pancreatic cancer patients. Histological analysis has shown that IGF-I receptor (IGF-IR) is positive in the membrane of pancreatic cancer tissues. These facts suggest that IGF-I acts as a growth factor for pancreatic cancer and inhibition of its action might be a good candidate for molecular therapy of pancreatic cancer. A possible problem is that not all pancreatic cancers produce IGF-I, which might be a reason for ineffective results of its clinical application.

A research team from Japan have proved that inhibition of IGF-IR activity results in a decrease in proliferation and motility of pancreatic cancer cell lines. Their study will be published on April 21, 2010 in the World Journal of Gastroenterology.

Their study indicated that IGF-IR was expressed and played a role in proliferation and motility of pancreatic cancer cell lines. Further analysis of this phenomenon could unveil a new role for a growth factor receptor and its downstream pathway in cancer. One possible mechanism would be that the downstream pathway stimulates its upstream receptor via some unknown molecule, like a retrograde flow.