Journal
CELL CYCLE
Volume 14, Issue 13, Pages 2149-2159Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/15384101.2015.1041688
Keywords
apoptosis; CLIPR-59; Glioma; RIP1; Spy1; TNF-alpha
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Funding
- National Basic Research Program of China (973 Program) [2012CB822104, 2011CB910604]
- National Natural Science Foundation of China [314440037, 31270802, 81272789, 81372687, 31300902]
- Priority Academic Program Development of Jiangsu Higher Education Institutions (PAPD)
- Colleges and Universities in Natural Science Research Project of Jiangsu Province [11KJA310002, 13KJB310009]
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Glioblastoma multiforme (GBM), a grade-IV glioma, is resistant to TNF- induced apoptosis. CLIPR-59 modulates ubiquitination of RIP1, thus promoting Caspase-8 activation to induce apoptosis by TNF-. 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-. These findings have identified a novel Spy1-CLIPR-59 interplay in GBM cell's resistance to TNF--induced apoptosis revealing a potential target in the intervention of malignant brain tumors.
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