Study summary · research use only
Vasoactive intestinal peptide: autocrine growth factor in neuroblastoma
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This study examined vasoactive intestinal peptide (VIP) receptor expression in human neuroblastoma. The authors report VIP receptors in 12 of 15 primary tumours by binding studies (KD = 1.3-12.4 nM) and VIP-stimulated adenylate cyclase, with the VIP stimulation index inversely correlated with tumour VIP content. In two human cell lines, IMR32 and SKNSH, both expressed high-affinity VIP receptors (KD = 4 nM and 2.5 nM). IMR32 cells had low VIP (0.6 pg/10(6) cells); exogenous VIP stimulated adenylate cyclase 22-fold and reduced IMR32 proliferation by 49% over 6 days. SKNSH cells had higher VIP (6.3 pg/10(6) cells) and lower VIP-stimulated cyclase, with minimally changed proliferation. The authors interpret this as supporting a VIP autocrine role in neuroblastoma.
Abstract
Neuroblastoma is the most common solid tumor of children less than 5 years of age; yet the biology of this tumor is poorly understood. Neuroblastoma tumors are derived from neural crest precursors; they synthesize both adrenergic and peptidergic neurotransmitters. This study determined VIP receptor expression in primary neuroblastoma tumors prior to chemotherapy. The VIP receptor was expressed in 12 of 15 neuroblastoma tumors as determined by direct binding studies (KD = 1.3-12.4 nM) and VIP-mediated stimulation of adenylate cyclase. The VIP stimulation index for adenylate cyclase in the primary tumor was inversely correlated with the VIP content of the tumor, suggesting that VIP regulates its own receptor expression. Similar observations were made in vitro by comparison of two human neuroblastoma cell lines, IMR32 and SKNSH. Both cell lines were demonstrated to express specific, high affinity VIP receptors (KD = 4 nM and 2.5 nM for IMR32 and SKNSH, respectively). IMR32 cells contained very low levels of VIP (0.6 pg VIP/10(6) cells). Exogenous VIP stimulated adenylate cyclase 22-fold over basal activity and VIP inhibited proliferation of IMR32 cells by 49% in 6-day cultures. On the other hand, SKNSH cells synthesized high levels of VIP (6.3 pg/10(6) cells), metabolized VIP rapidly and demonstrated a low level of VIP-mediated stimulation of adenylate cyclase; their proliferation rate was minimally inhibited by exogenous VIP. These observations help validate the hypothesis that VIP serves as an autocrine growth factor in neuroblastoma.
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