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VPAC 1 Receptors and Lung Cancer
Author(s) -
MOODY T. W.,
WALTERS J.,
CASIBANG M.,
ZIA F.,
GOZES Y.
Publication year - 2000
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2000.tb06947.x
Subject(s) - lung cancer , autocrine signalling , cancer , melanoma , cancer research , receptor , prostate cancer , cancer cell , agonist , cell culture , microbiology and biotechnology , medicine , biology , endocrinology , genetics
A bstract : VIP/PACAP are autocrine growth factors for lung cancer. VIP and/or PACAP mRNA is present in most lung cancer cell lines examined. Although mRNA for VPAC 2 ‐R is not common, VPAC 1 ‐R and PAC 1 ‐R mRNA is present in many lung cancer cell lines. 125 I‐VIP binds with high affinity to lung cancer cells and specific 125 I‐VIP binding is inhibited with high affinity by (Lys 15 , Arg 16 , Leu 27 )VIP 1–7 GRF8–27, the VPAC 1 ‐R specific agonist, but not by Ro25–1553 18 , the VPAC 2 ‐R specific agonist. VIP elevates cAMP and increases c‐fos gene expression. The increase in cAMP and c‐fos mRNA caused by VIP is inhibited by SN(VH). (SH)VH inhibited the proliferation of NCI‐H1299 cells in the MTT assay, which is based on cytotoxicity. In a recent cell line screen, (SN)VH inhibited the growth of 51 of 56 cancer cell lines including leukemia, lung cancer, colon cancer, CNS cancer, melanoma, ovarian cancer, renal cancer, breast cancer, and prostate cancer (T. Moody, unpublished). It remains to be determined if (SN)VH will be useful for treatment of a wide variety of cancers.