ArticleJournal of neuro-oncology2007
Dual targeting of IGF-1R and PDGFR inhibits proliferation in high-grade gliomas cells and induces radiosensitivity in JNK-1 expressing cells.
Article in Journal of neuro-oncology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
20 citing papers in PubMed, 35 citations in OpenAlex.
- Redundancy in Growth Factor Receptor Signaling in Adult Astrocytoma Resistance to Small-Molecule Tyrosine Kinase Inhibitors.International journal of molecular sciences · 2026Review
- A Review of FDA-Approved Multi-Target Angiogenesis Drugs for Brain Tumor Therapy.International journal of molecular sciences · 2025Review
- Article
- Advancements, Challenges, and Future Directions in Tackling Glioblastoma Resistance to Small Kinase Inhibitors.Cancers · 2022Review
- The Interference between SARS-CoV-2 and Tyrosine Kinase Receptor Signaling in Cancer.International journal of molecular sciences · 2021Review
- Receptor tyrosine kinase targeting in glioblastoma: performance, limitations and future approaches.Contemporary oncology (Poznan, Poland) · 2020Review
- Platelet-Derived Growth Factor Receptor and Ionizing Radiation in High Grade Glioma Cell Lines.International journal of molecular sciences · 2019Article
- PDGFR and IGF-1R Inhibitors Induce a G2/M Arrest and Subsequent Cell Death in Human Glioblastoma Cell Lines.Cells · 2018Article
- The Influence of EGFR Inactivation on the Radiation Response in High Grade Glioma.International journal of molecular sciences · 2018Article
- Targeting the VEGF and PDGF signaling pathway in glioblastoma treatment.International journal of clinical and experimental pathology · 2015Article
- Plasma levels of glucose and insulin in patients with brain tumors.Current health sciences journal · 2014Article
- Modulation of insulin-like growth factor-1 receptor and its signaling network for the treatment of cancer: current status and future perspectives.Oncology reviews · 2013Review
- The insulin-like growth factor system in cancer.Endocrinology and metabolism clinics of North America · 2012Review
- Novel therapeutic targets in the brain tumor microenvironment.Oncotarget · 2012Article
- Heparan sulfate sulfatase SULF2 regulates PDGFRα signaling and growth in human and mouse malignant glioma.The Journal of clinical investigation · 2012Article
- Role of IGF-1 receptor in radiation response.Translational oncology · 2012Article
- Insulin-like growth factor: current concepts and new developments in cancer therapy.Recent patents on anti-cancer drug discovery · 2012Review
- Helianthin induces antiproliferative effect on human glioblastoma cells in vitro.Journal of neuro-oncology · 2011Article
- Effects of irradiation on tumor cell survival, invasion and angiogenesis.Journal of neuro-oncology · 2010Review
- Effect of VEGFR, PDGFR and PI3K/mTOR Targeting in Glioblastoma.Current health sciences journalArticle
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Increased expression and activation of receptor tyrosine kinases frequently occur in human brain tumors, mediating a variety of growth-promoting pathways and leading to radioresistance; however, little is known about their motogenic potency relative to one another. In this study, we found co-expression of Insulin like growth factor-1 receptor (IGF-1R) and platelet derived growth factor receptor (PDGFR) in two high-grade gliomas (HGG) cell lines 18 and 38. Dual targeting of IGF-1R and PDGFR increased cell death in both 18 and 38 cell lines in comparison to inhibition of either receptor alone. In addition, co-inhibition of IGF-1R and PDGFR increased radiosensitivity in 18 cells but failed to intensify the effect of radiation in 38 cells. In HGG cells, radiation-induced cell death has been connected to the activation of c-Jun-NH2-terminal kinase-1 (JNK1). We found that JNK1 was weakly expressed in 38 cells while it had an elevated expression in 18 cells. Exposure to ionizing radiation induced JNK1 activation only in 18 cells without affecting the protein activity in 38 cells. These results suggest that in 18 cell line radiation-activated JNK1 may provide an anti-proliferative signaling, parallel to receptors co-targeting. To test this hypothesis, HGG cells were treated with dominant negative JNK1 (dnJNK1) and the response to radiation was assayed in presence or absence of receptors co-inhibition. Indeed dnJNK protected 18 cells against gamma-irradiation-induced cell death. dnJNK treatment did not influence radiation response of the 38 cell line, which expressed low levels of JNK1. In conclusion we found that IGF-1R and PDGFR co-inhibition caused an increased cell death in two HGG cell line and induced the radiosensitization of the JNK1 expressing cell line.
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