ArticleOncogene2007
Inhibition of IGF-I receptor in anchorage-independence attenuates GSK-3beta constitutive phosphorylation and compromises growth and survival of medulloblastoma cell lines.
Article in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 38 citations in OpenAlex.
- Drugging Hijacked Kinase Pathways in Pediatric Oncology: Opportunities and Current Scenario.Pharmaceutics · 2023Review
- Polymorphisms of insulin receptor substrate 2 are putative biomarkers for pediatric medulloblastoma: considering the genetic susceptibility and pathological diagnoses.Nagoya journal of medical science · 2017Article
- Type I insulin-like growth factor receptor signaling in hematological malignancies.Oncotarget · 2017Review
- The selective PI3Kα inhibitor BYL719 as a novel therapeutic option for neuroendocrine tumors: Results from multiple cell line models.PloS one · 2017Article
- BDNF/TrkB Signaling as a Potential Novel Target in Pediatric Brain Tumors: Anticancer Activity of Selective TrkB Inhibition in Medulloblastoma Cells.Journal of molecular neuroscience : MN · 2016Article
- Activation of glycogen synthase kinase 3β ameliorates diabetes-induced kidney injury.The Journal of biological chemistry · 2014Article
- GSK-3 as potential target for therapeutic intervention in cancer.Oncotarget · 2014Review
- IGF-1R, a target of let-7b, mediates crosstalk between IRS-2/Akt and MAPK pathways to promote proliferation of oral squamous cell carcinoma.Oncotarget · 2014Article
- GSK3β regulates physiological migration of stem/progenitor cells via cytoskeletal rearrangement.The Journal of clinical investigation · 2013Article
- Targeting the insulin-like growth factor-1 receptor in human cancer.Frontiers in pharmacology · 2013Article
- Regulation of apoptosis by the circadian clock through NF-kappaB signaling.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- ROS accumulation and IGF-IR inhibition contribute to fenofibrate/PPARalpha -mediated inhibition of glioma cell motility in vitro.Molecular cancer · 2010Article
- IGF-IR-dependent expression of Survivin is required for T-antigen-mediated protection from apoptosis and proliferation of neural progenitors.Cell death and differentiation · 2010Article
- Treatment of biliary tract cancer with NVP-AEW541: mechanisms of action and resistance.World journal of gastroenterology · 2010Article
- Disease evidence for IGFBP-2 as a key player in prostate cancer progression and development of osteosclerotic lesions.American journal of translational research · 2009Article
- IGF-IR in neuroprotection and brain tumors.Frontiers in bioscience (Landmark edition) · 2009Review
- Glycogen synthase kinase 3beta induces apoptosis in cancer cells through increase of survivin nuclear localization.Cancer letters · 2008Article
- Biological background of pediatric medulloblastoma and ependymoma: a review from a translational research perspective.Neuro-oncology · 2008Review
- Activation of PPARalpha inhibits IGF-I-mediated growth and survival responses in medulloblastoma cell lines.International journal of cancer · 2008Article
- Developmental expression and differentiation-related neuron-specific splicing of metastasis suppressor 1 (Mtss1) in normal and transformed cerebellar cells.BMC developmental biology · 2007Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 3 countries.
Funding
Abstract
We have previously reported that insulin-like growth factor-I (IGF-I) supports growth and survival of mouse and human medulloblastoma cell lines, and that IGF-I receptor (IGF-IR) is constitutively phosphorylated in human medulloblastoma clinical samples. Here, we demonstrate that a specific inhibitor of insulin-like growth factor-I receptor (IGF-IR), NVP-AEW541, attenuated growth and survival of mouse (BsB8) and human (D384, Daoy) medulloblastoma cell lines. Cell cycle analysis demonstrated that G1 arrest and apoptosis contributed to the action of NVP-AEW54. Interestingly, very aggressive BsB8 cells, which derive from cerebellar tumors of transgenic mice expressing viral oncoprotein (large T-antigen from human polyomavirus JC) became much more sensitive to NVP-AEW541 when exposed to anchorage-independent culture conditions. This high sensitivity to NVP-AEW54 in suspension was accompanied by the loss of GSK-3beta constitutive phosphorylation and was independent from T-antigen-mediated cellular events (Supplementary Materials). BsB8 cells were partially rescued from NVP-AEW541 by GSK3beta inhibitor, lithium chloride and were sensitized by GSK3beta activator, sodium nitroprusside (SNP). Importantly, human medulloblastoma cells, D384, which demonstrated partial resistance to NVP-AEW541 in suspension cultures, become much more sensitive following SNP-mediated GSK3beta dephosphorylation (activation). Our results indicate that hypersensitivity of medulloblastoma cells in anchorage-independence is linked to GSK-3beta activity and suggest that pharmacological intervention against IGF-IR with simultaneous activation of GSK3beta could be highly effective against medulloblastomas, which have intrinsic ability of disseminating the CNS via cerebrospinal fluid.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.