ArticleCell cycle (Georgetown, Tex.)2015
Spy1 induces de-ubiquitinating of RIP1 arrest and confers glioblastoma's resistance to tumor necrosis factor (TNF-α)-induced apoptosis through suppressing the association of CLIPR-59 and CYLD.
Article in Cell cycle (Georgetown, Tex.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 24 citations in OpenAlex.
- ACT001 synergizes with temozolomide-based chemoradiotherapy to cure refractory glioblastoma by targeting TNF-CXCL10-CD8Frontiers in pharmacology · 2026Article
- Novel tumor necrosis factor-related long non-coding RNAs signature for risk stratification and prognosis in glioblastoma.Frontiers in neurology · 2023Article
- Golgi Complex: A Signaling Hub in Cancer.Cells · 2022Review
- Downregulated CLIP3 induces radioresistance by enhancing stemness and glycolytic flux in glioblastoma.Journal of experimental & clinical cancer research : CR · 2021Article
- Targeting the Ubiquitin System in Glioblastoma.Frontiers in oncology · 2020Review
- Suppression of the Smurf1 Expression Inhibits Tumor Progression in Gliomas.Cellular and molecular neurobiology · 2018Article
- IGFBP6 Regulates Cell Apoptosis and Migration in Glioma.Cellular and molecular neurobiology · 2017Article
- Hck Promotes Neuronal Apoptosis Following Intracerebral Hemorrhage.Cellular and molecular neurobiology · 2017Article
- Speedy A-Cdk2 binding mediates initial telomere-nuclear envelope attachment during meiotic prophase I independent of Cdk2 activation.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- CYLD downregulates Livin and synergistically improves gemcitabine chemosensitivity and decreases migratory/invasive potential in bladder cancer: the effect is autophagy-associated.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- The Expression of VHL (Von Hippel-Lindau) After Traumatic Spinal Cord Injury and Its Role in Neuronal Apoptosis.Neurochemical research · 2016Article
- miR-130b, an onco-miRNA in bladder cancer, is directly regulated by NF-κB and sustains NF-κB activation by decreasing Cylindromatosis expression.Oncotarget · 2016Article
- Spy1 participates in the proliferation and apoptosis of epithelial ovarian cancer.Journal of molecular histology · 2016Article
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Authors and funding
10 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma multiforme (GBM), a grade-IV glioma, is resistant to TNF-α induced apoptosis. CLIPR-59 modulates ubiquitination of RIP1, thus promoting Caspase-8 activation to induce apoptosis by TNF-α. Here we reported that CLIPR-59 was down-regulated in GBM cells and high-grade glioma tumor samples, which was associated with decreased cancer-free survival. In GBM cells, CLIPR-59 interacts with Spy1, resulting in its decreased association with CYLD, a de-ubiquitinating enzyme. Moreover, experimental reduction of Spy1 levels decreased GBM cells viability, while increased the lysine-63-dependent de-ubiquitinating activity of RIP1 via enhancing the binding ability of CLIPR-59 and CYLD in GBM, thus promoting Caspase-8 and Caspase-3 activation to induce apoptosis by TNF-α. These findings have identified a novel Spy1-CLIPR-59 interplay in GBM cell's resistance to TNF-α-induced apoptosis revealing a potential target in the intervention of malignant brain tumors.
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