GRP receptors are present in non small cell lung cancer cells

Previously, GRP receptors wer charachterized in sasmll cell lung cancer cells and here non‐small cell lung cancer (NSCLC) cells were investigated: (125I‐Tyr4) bombesin (BN) or 125I‐GRP bound with high affinity to NCI‐H720 (lung carcioid) and NCI‐H1299 (large cell carcinoma) cells. Binding was specific, time dependent, and saturable. Specific (125I‐Tyr4) BN binding to NCI‐H1299 cells was inhibited with high affinity by GRP, BN, GRP14–27, (D‐Phe6)BN6–13methyl ester, moderate affinity by NMB, and low affinity by NMB, and low, and low affinity by GRP1–16. BN (10nM) transiently elevated cytosolic calcium in a dose dependent manner. BN caused translocation of protein kinase C from the cytosol to the membrane and the translocation caused by BN was reversed by (D‐Phe6)BN6–13 methylester. BN stimulated arachidonic acid release and the increase caused by BN was reversed by (D‐Phe6)BN6–13 methylester. Using a clonogenic assay, BN stimulated the growth of NCI‐H720 cells, and ythe number of colonies was reduced using (D‐Phe6)BN6–13 methylester. These data suggest that GRP receptors that are present in lung carcinoid and NSCLC cells may regulate proliferation. © 1996 Wiley‐Liss, Inc. This article is a US Government work and, as such, is in the public domain in the United States of America.