pepmg_

Study summary · research use only

A vasoactive intestinal peptide antagonist inhibits non-small cell lung cancer growth

Study · human · Proceedings of the National Academy of Sciences of the United States of America · 1993 · DOI 10.1073/pnas.90.10.4345 · PMID 8389448

Plain-language summary

Paraphrased from the published abstract below — not a verdict on whether anything works.

This study examined a vasoactive intestinal peptide (VIP) antagonist (VIP-hyb) on non-small cell lung cancer (NSCLC) growth in nude mice and cell lines. The abstract reports that when VIPhyb (10 micrograms, s.c.) was injected daily into nude mice, xenograft formation was reduced by approximately 80%. In vitro, VIP (100 nM) stimulated colony formation approximately 2-fold, while 1 microM VIPhyb reduced colony formation by approximately 50% in the NCI-H838 line. VIPhyb inhibited 125I-labeled VIP binding to NCI-H157 and NCI-H838 with an IC50 of 0.7 microM. VIP (10 nM) increased cAMP 5-fold in NCI-H838, and 10 microM VIPhyb reduced this increase. The authors suggest VIP may be a regulatory peptide in NSCLC and VIPhyb a VIP receptor antagonist.

Abstract

The most prevalent lung cancer, non-small cell lung cancer (NSCLC) has receptors for vasoactive intestinal peptide (VIP). Here the effects of a VIP antagonist (VIP-hyb) on NSCLC growth were investigated. In vivo, when VIPhyb (10 micrograms, s.c.) was daily injected into nude mice, xenograft formation was significantly inhibited by approximately 80%. In vitro, VIP (100 nM) stimulated colony formation approximately 2-fold, whereas 1 microM VIPhyb inhibited colony formation by approximately 50% when adenocarcinoma cell line NCI-H838 was used. The attenuation of tumor proliferation is receptor mediated, as VIPhyb inhibited specific 125I-labeled VIP binding to cell lines NCI-H157 and NCI-H838 with an IC50 of 0.7 microM. VIP (10 nM) increased the cAMP levels 5-fold when cell line NCI-H838 was used, and 10 microM VIPhyb inhibited the increase in cAMP caused by VIP. Northern blot analysis and radioimmunoassays have shown VIP mRNA and VIP-like immunoreactivity in NSCLC cells. These data suggest that VIP may be a regulatory peptide in NSCLC and that VIPhyb is a VIP receptor antagonist that inhibits proliferation.

Read the full study on PubMed ↗

pepmg summarizes the peer-reviewed literature and links to every source — it sells nothing, ships nothing, and gives no medical, dosing, or human-use guidance. Don't just trust this summary: follow the citation to its source and read it yourself. Research use only.