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Updated: Aug 9, 2026

Human Neuroendocrine Tumor Cell Lines as a Three-Dimensional Model for the Study of Human Neuroendocrine Tumor Therapy
12:04

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Published on: August 14, 2012

Somatostatin inhibits PDGF-stimulated Ras activation in human neuroblastoma cells

M G Cattaneo1, G Scita, L M Vicentini

  • 1Department of Pharmacology, University of Milano, Via Vanvitelli, 32, 20129, Milano, Italy.

FEBS Letters
|October 6, 1999
PubMed

Insights

Somatostatin (SST) inhibits tumor cell growth by blocking Ras activation. This occurs through decreased PDGF receptor phosphorylation, independent of pertussis toxin but dependent on peroxovanadate.

Area of Science:

  • Endocrinology
  • Oncology
  • Molecular Biology

Background:

  • Somatostatin (SST) primarily regulates hormone secretion.
  • SST exhibits antiproliferative effects on human tumors through direct and indirect pathways.
  • Previous studies showed SST analogue lanreotide inhibited neuroblastoma cell proliferation and MAP kinase activity.

Purpose of the Study:

  • To investigate the effect of Somatostatin (SST) on Platelet-Derived Growth Factor (PDGF)-induced Ras activation in human neuroblastoma cells.

Main Methods:

  • Utilized human neuroblastoma cell line SY5Y.
  • Examined PDGF-induced Ras activation and PDGF receptor phosphorylation.
  • Assessed the role of pertussis toxin (PTx) and peroxovanadate in SST's effects.
  • Measured Ras-specific GTPase activating protein (GAP) activities.

Main Results:

  • SST suppressed PDGF-induced Ras activation in a PTx-independent and peroxovanadate-dependent manner.
  • SST treatment did not alter Ras-specific GAP activities.
  • PDGF-induced PDGF receptor phosphorylation was decreased by SST, explaining the inhibition of Ras activation.

Conclusions:

  • SST inhibits PDGF-induced Ras activation in neuroblastoma cells.
  • The mechanism involves the downregulation of PDGF receptor phosphorylation.
  • These findings contribute to understanding SST's antiproliferative role in cancer therapy.

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