Abstract
Background: Somatostatin inhibits cell growth by interacting with somatostatin receptors (SSTRs). Functional SSTRs are lost during progression of pancreatic cancer. We hypothesized that reintroduction of SSTR-1 and -2 could cause pancreatic cancer cell cycle arrest in response to somatostatin. Methods: A SSTR-negative human pancreatic cancer cell line (Panc-1) was co-transfected with SSTR-1 and -2, and treated with somatostatin analog. The expression of SSTR-1 and -2 in transfected and untransfected Panc-1 cells was examined by quantitative real time PCR and flow cytometry.
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