Somatostatin analog RC-160 inhibits growth of CFPAC-1 human pancreatic cancer cells in vitro and intracellular production of cyclic adenosine monophosphate
✍ Scribed by Yunfcng Qin; Tibor Ertl; Kate Groot; Judit Horvath; Ren-Zhi Cai; Andrew V. Schally
- Publisher
- John Wiley and Sons
- Year
- 1995
- Tongue
- French
- Weight
- 832 KB
- Volume
- 60
- Category
- Article
- ISSN
- 0020-7136
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✦ Synopsis
The effect of somatostatin analog RC-I60 on the growth of CFPAC-I human pancreatic cancer cells in vitro was investigated. RC-I60 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 pM) RC-160, the cell number being decreased by 38% and 46%, respectively. RC-I60 was more potent than SS-14 or SMS2O I -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 55-14 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 [1251]-Tyr1'-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-I60 could bind to somatostatin receptors on these cells with an affinity similar to SS-14 but significantly higher than that of SMS2O 1-995. Radioimmunoassay of intracel-Mar CAMP showed that RC-I60 could powerfully inhibit forskotin-stimulated CAMP production in CFPAC-I cells. Addition of forskolin to the cultures increased CAMP concentrations in the cellular lysate of treated cells. RC-I60 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.