| Autor: |
Ding Z; a Jiangsu Province Key Laboratory for Inflammation and Molecular Drug Target; Nantong University ; Nantong , Jiangsu , PR China., Liu Y, Yao L, Wang D, Zhang J, Cui G, Yang X, Huang X, Liu F, Shen A |
| Jazyk: |
angličtina |
| Zdroj: |
Cell cycle (Georgetown, Tex.) [Cell Cycle] 2015; Vol. 14 (13), pp. 2149-59. Date of Electronic Publication: 2015 May 27. |
| DOI: |
10.1080/15384101.2015.1041688 |
| Abstrakt: |
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. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
|
