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Inhibition of human neuroblastoma growth by a specific VIP antagonist
G Lilling1, Y Wollman, M N Goldstein
1Department of Clinical Biochemistry, Sackler School of Medicine, Tel Aviv University, Israel.
Abstract:
The 28-amino-acid neuropeptide, vasoactive intestinal peptide (VIP), is a potent mitogen during embryonic development and plays a vital role in brain growth. VIP is also mitogenic for tumor cells, including the human neuroblastoma (NMB). Northern blot analysis has revealed VIP mRNA transcripts in NMB. We now report VIP-like immunoreactivity within these neuroblastoma cells that increased during logarithmic growth and decreased after attaining confluency. About 10(6) seeded cells secreted 5-40 pg of VIP-like immunoreactivity into the medium. These results suggest an autocrine role for VIP in the regulation of neuroblastoma growth. A VIP hybrid antagonist (neurotensin6-11 VIP7-28) that has been shown to inhibit lung cancer proliferation was now tested for inhibition of neuroblastoma growth. Receptor binding studies indicated that the hybrid antagonist displaced [125I]-VIP binding in the neuroblastoma cells (EC50 = 5 x 10(-6)M). Furthermore, as measured by thymidine incorporation and by cell counts, the potent VIP hybrid antagonist inhibited neuroblastoma multiplication in a dose-dependent manner. In conclusion, VIP may be an important regulator of growth of nerve cell progenitors and of tumors derived from neuronal origin and intervening with VIP function may lead to improved treatment of cancer.
Insights
Vasoactive intestinal peptide (VIP) fuels neuroblastoma growth, acting as an autocrine factor. A novel VIP antagonist effectively inhibited neuroblastoma cell proliferation, suggesting a new cancer treatment strategy.
Area of Science:
- Neuroscience
- Oncology
- Molecular Biology
Background:
- Vasoactive intestinal peptide (VIP) is a neuropeptide crucial for embryonic development and brain growth.
- VIP also exhibits mitogenic properties for tumor cells, including human neuroblastoma (NMB).
- Previous studies detected VIP mRNA transcripts in neuroblastoma cells.
Purpose of the Study:
- To investigate the role of VIP in neuroblastoma growth.
- To evaluate the efficacy of a VIP hybrid antagonist in inhibiting neuroblastoma proliferation.
Main Methods:
- Northern blot analysis to detect VIP mRNA.
- Measurement of VIP-like immunoreactivity in neuroblastoma cells and culture medium.
- Receptor binding assays using [125I]-VIP.
- Assessment of cell proliferation via thymidine incorporation and cell counts.
Main Results:
- VIP-like immunoreactivity was found in neuroblastoma cells, increasing with growth and decreasing at confluency.
- Neuroblastoma cells secreted VIP-like immunoreactivity into the medium, suggesting autocrine signaling.
- A VIP hybrid antagonist displaced [125I]-VIP binding and dose-dependently inhibited neuroblastoma cell multiplication.
Conclusions:
- VIP appears to play an autocrine role in regulating neuroblastoma growth.
- VIP signaling is a potential therapeutic target for neuroblastoma and other neuronal-derived tumors.
- VIP hybrid antagonists show promise for inhibiting neuroblastoma proliferation.
