ArticleJournal of molecular neuroscience : MN2019
Inhibition of Ubc9-Induced CRMP2 SUMOylation Disrupts Glioblastoma Cell Proliferation.
Article in Journal of molecular neuroscience : MN, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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
9 citing papers in PubMed, 17 citations in OpenAlex.
- Targeting SUMOylation in glioblastoma: A novel avenue for therapy and biomarker discovery.Genes & diseases · 2026Review
- Dual Regulation of Post-Translational Modification of Proteins: Bottlenecks and Breakthroughs in NK Cell Therapy for Glioblastoma.International journal of general medicine · 2026Review
- Elevated UBC9 expression and its oncogenic role in colorectal cancer progression and chemoresistance.Scientific reports · 2025Article
- Targeted inhibition of SUMOylation: treatment of tumors.Human cell · 2024Review
- The emerging roles of SUMOylation in the tumor microenvironment and therapeutic implications.Experimental hematology & oncology · 2023Review
- Positioning SUMO as an immunological facilitator of oncolytic viruses for high-grade glioma.Frontiers in cell and developmental biology · 2023Review
- Proteo-transcriptomics meta-analysis identifies SUMO2 as a promising target in glioblastoma multiforme therapeutics.Cancer cell international · 2021Article
- The Molecular Basis of Ubiquitin-Conjugating Enzymes (E2s) as a Potential Target for Cancer Therapy.International journal of molecular sciences · 2021Review
- SUMOylation Regulator-Related Molecules Can Be Used as Prognostic Biomarkers for Glioblastoma.Frontiers in cell and developmental biology · 2021Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Glioblastoma (GBM) is the most aggressive astrocytoma. Despite maximum treatment, the GBM usually recurs and the patient survival is poor. Thus, understanding the molecular mechanism of GBM progression will be meaningful to ameliorate this situation. In this study, collapsin response mediator protein 2 (CRMP2) and Ubc9 protein levels were evaluated in three GBM cell lines. Sumoylated CRMP2 were enriched and immunoprecipitated using SUMO1 and IgG antibodies. CRMP2-K374A mutant was generated by site-direct mutagenesis. All indicated constructs were transfected into GL15 cells, and the corresponding proliferation-promoting effect was assessed through cell proliferation ratio. The t-CSM peptide was used to disturb Ubc9-CRMP2 interaction. CRMP2 is expressed in all tested GBM cell lines. The Ubc9 protein levels are positively correlated with CRMP2 level, and both can promote GBM cell proliferation. Blocking CRMP2 SUMOylation through SUMOylation-incompetent mutant or small peptide suppresses CRMP2-induced GBM cell proliferation. This study demonstrates that the CRMP2 SUMOylation exists widely in GBM cells and drives glioblastoma proliferation. CRMP2 SUMOylation inhibition can significantly suppress GBM proliferation in vitro.
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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 Socratic graph.