The effect of somatostatin analog RC‐160 on the growth of CFPAC‐I human pancreatic cancer cells in vitro was investigated. RC‐160 effectively inhibited the proliferation of CFPAC‐I cells in culture, inducing a time‐ and dose‐dependent decrease in the number of treated cells. A significant suppression of cell growth was observed after 48 and 72 hr of the exposure to (I μM) RC‐160, the cell number being decreased by 38% and 46%, respectively. RC‐160 was more potent than SS‐14 or SMS201–995 in inhibiting the growth of CFPAC‐I cells, and after 48‐hr treatment the cell number decreased by 49% for RC‐160 compared with 12% for SS‐14 and 27% for SMS201‐995. Binding experiments demonstrated that specific receptors for somatostatin were present on CFPAC‐I cells. SS‐14 showed a high binding affinity for [125I]‐Tyr11‐SS‐14 receptors on CFPAC‐I cells. Scatchard analysis indicated the presence of 2 classes of somatostatin binding sites on the cells, one with high binding affinity and low capacity and the other with low binding affinity and high capacity. RC‐160 could bind to somatostatin receptors on these cells with an affinity similar to SS‐14 but significantly higher than that of SMS201–995. Radioimmunoassay of intracellular cAMP showed that RC‐160 could powerfully inhibit forskolin‐stimulated cAMP production in CFPAC‐I cells. Addition of forskolin to the cultures increased cAMP concentrations in the cellular lysate of treated cells. RC‐160 attenuated or nullified in a dose‐dependent manner the cAMP production stimulated by forskolin. Our observations indicate that somatostatin analog RC‐160 inhibits the proliferation of CFPAC‐I human pancreatic cancer cells in vitro and that this effect may involve the intracellular cAMP pathway.
ASJC Scopus subject areas
- Cancer Research