ArticleThe American journal of pathology1999
Up-regulation of insulin-like growth factor-II expression is a feature of TrkA but not TrkB activation in SH-SY5Y neuroblastoma cells.
Article in The American journal of pathology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 43 citations in OpenAlex.
- Advances in Targeting Growth Factor Signalling in Neuroblastoma and Overcoming Drug Resistance.Cells · 2025Review
- Comparison of tyrosine kinase domain properties for the neurotrophin receptors TrkA and TrkB.The Biochemical journal · 2020Article
- Two Receptors, Two Isoforms, Two Cancers: Comprehensive Analysis of KIT and TrkA Expression in Neuroblastoma and Acute Myeloid Leukemia.Frontiers in oncology · 2019Article
- Constitutively active TrkB confers an aggressive transformed phenotype to a neural crest-derived cell line.Oncogene · 2014Article
- Clinical significance of NTRK family gene expression in neuroblastomas.Pediatric blood & cancer · 2012Article
- NGF activation of TrkA induces vascular endothelial growth factor expression via induction of hypoxia-inducible factor-1α.Molecular and cellular neurosciences · 2011Article
- The connections between neural crest development and neuroblastoma.Current topics in developmental biology · 2011Review
- On Trk--the TrkB signal transduction pathway is an increasingly important target in cancer biology.Clinical cancer research : an official journal of the American Association for Cancer Research · 2009Review
- Brain-derived neurotrophic factor modulates expression of chemokine receptors in the brain.Brain research · 2008Article
- Article
- The IGF/IGFBP system in CNS malignancy.Molecular pathology : MP · 2001Review
- Exercise as Gene Therapy: BDNF and DNA Damage Repair.Asia-Pacific journal of ophthalmology (Philadelphia, Pa.)Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The types of neurotrophin receptors that are expressed in neuroblastomas have different prognostic implications; trkA is a marker of good prognosis, whereas trkB expression is associated with poor prognosis. This suggests that either the signaling that is mediated via these receptors modulates the biological features of neuroblastoma cells differently, or that distinct lineages of sympathoadrenal precursors have been transformed. In this report, we evaluate the biological effects after activation of trkA or trkB by their major ligands in SH-SY5Y human neuroblastoma cells. Both trkA and trkB induce differentiation, inhibit growth, and promote the survival of cells under conditions of nutrient deprivation. However, the up-regulation of insulin-like growth factor-II (IGF-II) expression is a predominant feature of trkA activation by nerve growth factor (NGF). The growth inhibition induced by blocking the insulin-like growth factor-I receptor suggests that IGF-II is a component of the effector mechanism of trkA activation by NGF in trkA-transfected cells. Although trkA and trkB expression is associated with different prognoses in neuroblastoma, our study indicates that the effects mediated by these receptors in vivo may be quite similar for certain subsets of neuroblastomas.
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