ArticleCancer science2013
Small ubiquitin-like modifier 1-3 conjugation [corrected] is activated in human astrocytic brain tumors and is required for glioblastoma cell survival.
Article in Cancer science, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 38 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.
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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
38 citing papers in PubMed, 59 citations in OpenAlex.
- RNA Modifications in Health and Disease.MedComm · 2025Review
- Post-translational modifications in DNA damage repair: mechanisms underlying temozolomide resistance in glioblastoma.Oncogene · 2025Review
- Population Studies and Molecular Mechanisms of Human Radioadaptive Capabilities: Is It Time to Rethink Radiation Safety Standards?International journal of molecular sciences · 2024Review
- Construction and validation of a prognostic nine-gene signature associated with radiosensitivity in head and neck squamous cell carcinoma.Clinical and translational radiation oncology · 2023Article
- Heat shock protein 27 deficiency promotes ferrous ion absorption and enhances acyl-Coenzyme A synthetase long-chain family member 4 stability to promote glioblastoma cell ferroptosis.Cancer cell international · 2023Article
- Positioning SUMO as an immunological facilitator of oncolytic viruses for high-grade glioma.Frontiers in cell and developmental biology · 2023Review
- Review
- Prognostic value, immune signature and molecular mechanisms of the SUMO family in pancreatic adenocarcinoma.Frontiers in molecular biosciences · 2022Article
- Proteo-transcriptomics meta-analysis identifies SUMO2 as a promising target in glioblastoma multiforme therapeutics.Cancer cell international · 2021Article
- Review
- Construction of a SUMOylation regulator-based prognostic model in low-grade glioma.Journal of cellular and molecular medicine · 2021Article
- SUMOylation of mitofusins: A potential mechanism for perinuclear mitochondrial congression in cells treated with mitochondrial stressors.Biochimica et biophysica acta. Molecular basis of disease · 2021Article
- Effects of targeting sumoylation processes during latent and induced Epstein-Barr virus infections using the small molecule inhibitor ML-792.Antiviral research · 2021Article
- SUMOylation of YTHDF2 promotes mRNA degradation and cancer progression by increasing its binding affinity with m6A-modified mRNAs.Nucleic acids research · 2021Article
- Current Status of SUMOylation Inhibitors.Current medicinal chemistry · 2021Review
- The Function of SUMOylation and Its Role in the Development of Cancer Cells under Stress Conditions: A Systematic Review.Stem cells international · 2020Review
- Zinc deficiency induces abnormal development of the myocardium by promoting SENP5 overexpression.PloS one · 2020Article
- Retinoid receptor turnover mediated by sumoylation, ubiquitination and the valosin-containing protein is disrupted in glioblastoma.Scientific reports · 2019Article
- SAE1 promotes human glioma progression through activating AKT SUMOylation-mediated signaling pathways.Cell communication and signaling : CCS · 2019Article
- SUMOylation in Glioblastoma: A Novel Therapeutic Target.International journal of molecular sciences · 2019Review
Corrections and comments
- Erratum issued
Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Small ubiquitin-like modifier (SUMO1-3) constitutes a group of proteins that conjugate to lysine residues of target proteins thereby modifying their activity, stability, and subcellular localization. A large number of SUMO target proteins are transcription factors and other nuclear proteins involved in gene expression. Furthermore, SUMO conjugation plays key roles in genome stability, quality control of newly synthesized proteins, proteasomal degradation of proteins, and DNA damage repair. Any marked increase in levels of SUMO-conjugated proteins is therefore expected to have a major impact on the fate of cells. We show here that SUMO conjugation is activated in human astrocytic brain tumors. Levels of both SUMO1- and SUMO2/3-conjugated proteins were markedly increased in tumor samples. The effect was least pronounced in low-grade astrocytoma (WHO Grade II) and most pronounced in glioblastoma multiforme (WHO Grade IV). We also found a marked rise in levels of Ubc9, the only SUMO conjugation enzyme identified so far. Blocking SUMO1-3 conjugation in glioblastoma cells by silencing their expression blocked DNA synthesis, cell growth, and clonogenic survival of cells. It also resulted in DNA-dependent protein kinase-induced phosphorylation of H2AX, indicative of DNA double-strand damage, and G(2) /M cell cycle arrest. Collectively, these findings highlight the pivotal role of SUMO conjugation in DNA damage repair processes and imply that the SUMO conjugation pathway could be a new target of therapeutic intervention aimed at increasing the sensitivity of glioblastomas to radiotherapy and chemotherapy.
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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.