ArticleMolecular neurobiology2018
CRMP2 Phosphorylation Drives Glioblastoma Cell Proliferation.
Article in Molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
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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
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.
- Sex-Specific Genetic Associations for Barrett's Esophagus and Esophageal Adenocarcinoma.Gastroenterology · 2020Pooled it
- Post-translational modifications of epigenetic modifier TIP60: their role in cellular functions and cancer.Epigenetics & chromatin · 2025Review
- Repurposing of nervous system drugs for cancer treatment: recent advances, challenges, and future perspectives.Discover oncology · 2025Review
- Drug Repurposing for Cancer Treatment: A Comprehensive Review.International journal of molecular sciences · 2024Review
- Genetic Analysis of Neurite Outgrowth Inhibitor-Associated Genes in Parkinson's Disease: A Cross-Sectional Cohort Study.CNS neuroscience & therapeutics · 2024Article
- CDK5: an oncogene or an anti-oncogene: location location location.Molecular cancer · 2023Review
- The evidence for repurposing anti-epileptic drugs to target cancer.Molecular biology reports · 2023Review
- The Contribution of Oxidative Stress toAntioxidants (Basel, Switzerland) · 2023Review
- Antitumor Potential of Antiepileptic Drugs in Human Glioblastoma: Pharmacological Targets and Clinical Benefits.Biomedicines · 2023Review
- CRMP2 as a Candidate Target to Interfere with Lung Cancer Cell Migration.Biomolecules · 2021Article
- Post-translational modifications of CDK5 and their biological roles in cancer.Molecular biomedicine · 2021Review
- Dihydropyrimidinase Like 2 Promotes Bladder Cancer Progression via Pyruvate Kinase M2-Induced Aerobic Glycolysis and Epithelial-Mesenchymal Transition.Frontiers in cell and developmental biology · 2021Article
- CRMP2 is a therapeutic target that suppresses the aggressiveness of breast cancer cells by stabilizing RECK.Oncogene · 2020Article
- Differential expression of Cdk5-phosphorylated CRMP2 following a spared nerve injury.Molecular brain · 2020Article
- Ketamine Regulates Phosphorylation of CRMP2 To Mediate Dendritic Spine Plasticity.Journal of molecular neuroscience : MN · 2020Article
- Anti-vimentin, anti-TUFM, anti-NAP1L1 and anti-DPYSL2 nanobodies display cytotoxic effect and reduce glioblastoma cell migration.Therapeutic advances in medical oncology · 2020Article
- Dynamic CRMP2 Regulation of CaV2.2 in the Prefrontal Cortex Contributes to the Reinstatement of Cocaine Seeking.Molecular neurobiology · 2020Article
- Inhibition of Ubc9-Induced CRMP2 SUMOylation Disrupts Glioblastoma Cell Proliferation.Journal of molecular neuroscience : MN · 2019Article
- Dysregulation of CRMP2 Post-Translational Modifications Drive Its Pathological Functions.Molecular neurobiology · 2019Review
- Protein tyrosine phosphatase 4A3 (PTP4A3/PRL-3) promotes the aggressiveness of human uveal melanoma through dephosphorylation of CRMP2.Scientific reports · 2019Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Glioblastoma (GBM) is an aggressive primary brain tumor. The rapid growth and the privileged provenance of the tumor within the brain contribute to its aggressivity and poor therapeutic targeting. A poor prognostic factor in glioblastoma is the deletion or mutation of the Nf1 gene. This gene codes for the protein neurofibromin, a tumor suppressor gene that is known to interact with the collapsin response mediator protein 2 (CRMP2). CRMP2 expression and elevated expression of nuclear phosphorylated CRMP2 have recently been implicated in cancer progression. The CRMP2-neurofibromin interaction protects CRMP2 from its phosphorylation by cyclin-dependent kinase 5 (Cdk5), an event linked to cancer progression. In three human glioblastoma cell lines (GL15, A172, and U87), we observed an inverse correlation between neurofibromin expression and CRMP2 phosphorylation levels. Glioblastoma cell proliferation was dependent on CRMP2 expression and phosphorylation by Cdk5 and glycogen synthase kinase 3 beta (GSK3β). The CRMP2 phosphorylation inhibitor (S)-lacosamide reduces, in a concentration-dependent manner, glioblastoma cell proliferation and induced apoptosis in all three GBM cell lines tested. Since (S)-lacosamide is bioavailable in the brain, we tested its utility in an in vivo orthotopic model of GBM using GL261-LucNeo glioma cells. (S)-lacosamide decreased tumor size, as measured via in vivo bioluminescence imaging, by ~54% compared to vehicle control. Our results introduce CRMP2 expression and phosphorylation as a novel player in GBM proliferation and survival, which is enhanced by loss of Nf1.
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What OpenQuestion holds
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.