Substance P activates responses correlated with tumour growth in human glioma cell lines bearing tachykinin NK1 receptors.

Abstract

The neuropeptide substance P (SP), by stimulating tachykinin NK1 receptors (NK1R), triggers a number of biological responses in human glioma cells which are potentially relevant for tumour growth. First, radioligand binding studies demonstrated the presence of tachykinin NK1R on SNB-19, DBTRG-05 MG and U373 MG, but not on U138 MG and MOG-G-GCM human glioma cell lines. Second, application of SP or neurokinin A (NKA) to NK1R+ glioma cell lines increased the secretion of interleukin 6 (IL-6) and potentiated IL-6 secretion induced by IL-1beta. SP also up-regulated the release of transforming growth factor beta1 (TGF-beta1) by the U373 MG glioma cell line. Third, SP induced new DNA synthesis and enhanced the proliferation rate of NK1R+, but not of NK1R- glioma cell lines. Also, NKA stimulated the proliferation and cytokine secretion in NK1R+ glioma cell lines. All the stimulant effects of SP/NKA on NK1R+ glioma cell lines were completely blocked by a specific tachykinin NK1R antagonist, MEN 11467. These data support the potential use of tachykinin NK1R antagonist for controlling the proliferative rate of human gliomas.

• Authors: C Palma, F Nardelli, S Manzini, C A Maggi
• Journal: British journal of cancer (Br J Cancer) Vol. 79 Issue 2 Pg. 236-43 (Jan 1999) ISSN: 0007-0920 [Print] England
• PMID: 9888463 (Publication Type: Journal Article)

Chemical References

• DNA, Neoplasm
• Interleukin-6
• Neoplasm Proteins
• Neurokinin-1 Receptor Antagonists
• Receptors, Neurokinin-1
• Transforming Growth Factor beta
• Interleukin-10
• Substance P
• Neurokinin A

Topics

• Cell Division (drug effects)
• DNA, Neoplasm (biosynthesis)
• Glioma (metabolism, pathology)
• Humans
• Interleukin-10 (metabolism)
• Interleukin-6 (metabolism)
• Neoplasm Proteins (drug effects, metabolism)
• Neurokinin A (pharmacology)
• Neurokinin-1 Receptor Antagonists
• Receptors, Neurokinin-1 (drug effects, metabolism)
• Substance P (antagonists & inhibitors, metabolism, pharmacology)
• Transforming Growth Factor beta (metabolism)
• Tumor Cells, Cultured (drug effects)