bc-264 and Glioma

Cholecystokinin (CCK) is known to stimulate cell proliferation but involvement of CCKB type receptors has not been exactly demonstrated so far. We examined the effect of CCK-8S and two receptor agonists on rat glioma C6 cells when using different CCKB receptor agonists and antagonists. Both CCK-8S and CCKB receptor agonists BC 264 and Suc-Trp-N(Me)Nle-Asp-Phe-NH2 stimulate [3H]thymidine incorporation. These effects were inhibited by CCKB receptor antagonist L-365,260 over 100-fold more effectively than it was seen by using CCKA receptor antagonist L-364,718. The data indicate that CCKB receptor agonists are potent stimulants of rat glioma C6 cell DNA synthesis suggesting that CCKB receptor activation is involved in cell proliferation within the central nervous system.

Topics: Amino Acid Sequence; Animals; Benzodiazepinones; Cell Division; Cholecystokinin; Devazepide; DNA; Glioma; Hormone Antagonists; Molecular Sequence Data; Oligopeptides; Peptide Fragments; Phenylurea Compounds; Rats; Receptors, Cholecystokinin; Sincalide; Thymidine; Tritium; Tumor Cells, Cultured