Abstract
The effect of pituitary adenylate cyclase activating polypeptide (PACAP) on small cell lung cancer (SCLC) cells was investigated. In Fura 2-AM loaded NCI-N417 cells, PACAP-27 or PACAP-38 elevated cytosolic calcium in a dose-dependent manner. The cytosolic calcium was elevated from 133 to 185 n M with PACAP-27 (100 n M). Because PACAP-27 strongly elevated cytosolic calcium after the addition of 1 m M EGTA, PACAP released calcium from intracellular pools using NCI-N417 cells; similar results were obtained for SCLC cell line NCI-H345. Pituitary adenylate cyclase activating polypeptide-27 inhibited 125I-VIP and 125I-PACAP binding to NCI-N417 cells with high affinity ( IC 50 = 30 and 5 n M), whereas VIP inhibited 125I-VIP and 125I-PACAP-27 binding with IC 50 values of 5 and 200 n M. Both 100 n M VIP and PACAP-27 elevated cAMP levels in NCI-H345 cells. In contrast, 1 μ M VIP had no effect on cytosolic calcium, whereas 100 n M PACAP-27 caused a strong calcium response. Both 100 n M VIP and 10 n M PACAP-27 significantly stimulated the clonal growth of NCI-H345 cells. These data suggest that biologically active VIP and PACAP receptors are present on SCLC cells.
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