ArticleThe Biochemical journal1988
Modulation of bombesin-induced phosphatidylinositol hydrolysis in a small-cell lung-cancer cell line.
Article in The Biochemical journal, 1988. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 43 citations in OpenAlex.
- P2-purinergic receptor agonists inhibit the growth of androgen-independent prostate carcinoma cells.The Journal of clinical investigation · 1992Article
- Review
- Bombesin, neuromedin B and neuromedin C interact with a common rat pancreatic phosphoinositide-coupled receptor, but are differentially regulated by guanine nucleotides.The Biochemical journal · 1991Article
- Neuropeptide growth factors and cancer.British journal of cancer · 1991Review
- Cholera toxin inhibits signal transduction by several mitogens and the in vitro growth of human small-cell lung cancer.The Journal of clinical investigation · 1990Article
- Neuropeptide stimulation of calcium flux in human lung cancer cells: delineation of alternative pathways.Proceedings of the National Academy of Sciences of the United States of America · 1990Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bombesin is an amphibian tetradecapeptide whose mammalian homologue, gastrin-releasing peptide (GRP), is produced by many small-cell lung-cancer (SCLC) cells, and which can function in an autocrine growth-promoting manner in SCLC. Studies reported here show that [Tyr4]bombesin and its congeners increase inositol 1,4,5-trisphosphate within seconds in NCI-H345, a SCLC cell line that constitutively produces GRP. After 30 min in the presence of 0.01 M-Li+ and [Tyr4]bombesin, there is marked accumulation of inositol monophosphates and inositol tetrakisphosphate. Pretreatment with phorbol 12-myristate 13-acetate (PMA) for 20 min inhibited the ability of [Tyr4]bombesin to induce phosphatidylinositol (PtdIns) turnover and to increase intracellular free Ca2+ ([Ca2+]i). Pretreatment with PMA for 48 h attenuated the ability of subsequently added PMA to decrease the response to [Tyr4]bombesin. Pretreatment with pertussis toxin (PT; 1 microgram/ml for 18-24 h) decreased by less than 30% [Tyr4]bombesin-induced increases in [Ca2+]i and PtdIns metabolites. However, interpretation of this result is complicated by the inability of PT to ADP-ribosylate completely its substrates in intact NCI-H345 cells. In contrast, pretreatment with cholera toxin (1 microgram/ml for 18-24 h) lowered basal [Ca2+]i and basal inositol phosphate concentrations, attenuated the response of NCI-H345 to subsequently added [Tyr4]bombesin, and was not mimicked by treatments that increase cellular cyclic AMP. These data demonstrate the activation of phospholipase C in SCLC by bombesin congeners. In addition, the results suggest a regulatory role for protein kinase C, a cholera-toxin substrate, and perhaps a pertussis-toxin substrate in the response of SCLC to bombesin.
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