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000127676 1001_ $$aKoschny, Ronald$$b0
000127676 245__ $$aBortezomib sensitizes primary meningioma cells to TRAIL-induced apoptosis by enhancing formation of the death-inducing signaling complex.
000127676 260__ $$aOxford$$bOxford University Press$$c2014
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000127676 520__ $$aA meningioma is the most common primary intracranial tumor in adults. Here, we investigated the therapeutic potential of the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in 37 meningiomas. Freshly isolated primary meningioma cells were treated with TRAIL with or without different sensitizing protocols, and apoptotic cell death was then quantified. Mechanisms of TRAIL sensitization were determined by a combination of Western blotting, flow cytometry, receptor complex immunoprecipitation, and siRNA-mediated knockdown experiments. Tumor necrosis factor-related apoptosis-inducing ligand receptor expression was analyzed using immunohistochemistry and quantified by an automated software-based algorithm. Primary tumor cells from 11 (29.7%) tumor samples were sensitive to TRAIL-induced apoptosis, 12 (32.4%) were intermediate TRAIL resistant, and 14 (37.8%) were completely TRAIL resistant. We tested synergistic apoptosis-inducing cotreatment strategies and determined that only the proteasome inhibitor bortezomib potently enhanced expression of the TRAIL receptors TRAIL-R1 and/or TRAIL-R2, the formation of the TRAIL death-inducing signaling complex, and activation of caspases; this treatment resulted in sensitization of all TRAIL-resistant meningioma samples to TRAIL-induced apoptosis. Bortezomib pretreatment induced NOXA expression and downregulated c-FLIP, neither of which caused the TRAIL-sensitizing effect. Native TRAIL receptor expression could not predict primary TRAIL sensitivity. This first report on TRAIL sensitivity of primary meningioma cells demonstrates that TRAIL/bortezomib cotreatment may represent a novel therapeutic option for meningiomas.
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000127676 650_7 $$2NLM Chemicals$$aAntineoplastic Agents
000127676 650_7 $$2NLM Chemicals$$aBoronic Acids
000127676 650_7 $$2NLM Chemicals$$aGRAMD4 protein, human
000127676 650_7 $$2NLM Chemicals$$aMitochondrial Proteins
000127676 650_7 $$2NLM Chemicals$$aPyrazines
000127676 650_7 $$2NLM Chemicals$$aTNF-Related Apoptosis-Inducing Ligand
000127676 650_7 $$2NLM Chemicals$$aTNFSF10 protein, human
000127676 650_7 $$069G8BD63PP$$2NLM Chemicals$$aBortezomib
000127676 7001_ $$aBoehm, Christina$$b1
000127676 7001_ $$0P:(DE-HGF)0$$aSprick, Martin R$$b2
000127676 7001_ $$aHaas, Tobias L$$b3
000127676 7001_ $$aHolland, Heidrun$$b4
000127676 7001_ $$aXu, Li-Xin$$b5
000127676 7001_ $$aKrupp, Wolfgang$$b6
000127676 7001_ $$aMueller, Wolf C$$b7
000127676 7001_ $$aBauer, Manfred$$b8
000127676 7001_ $$aKoschny, Thomas$$b9
000127676 7001_ $$aKeller, Marius$$b10
000127676 7001_ $$aSinn, Peter$$b11
000127676 7001_ $$aMeixensberger, Juergen$$b12
000127676 7001_ $$0P:(DE-HGF)0$$aWalczak, Henning$$b13
000127676 7001_ $$aGanten, Tom M$$b14
000127676 773__ $$0PERI:(DE-600)2033048-0$$a10.1097/NEN.0000000000000129$$gVol. 73, no. 11, p. 1034 - 1046$$n11$$p1034 - 1046$$tJournal of neuropathology and experimental neurology$$v73$$x1554-6578$$y2014
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