| pubmed-article:15711939 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15711939 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
| pubmed-article:15711939 | lifeskim:mentions | umls-concept:C0017638 | lld:lifeskim |
| pubmed-article:15711939 | lifeskim:mentions | umls-concept:C1367731 | lld:lifeskim |
| pubmed-article:15711939 | lifeskim:mentions | umls-concept:C1150587 | lld:lifeskim |
| pubmed-article:15711939 | lifeskim:mentions | umls-concept:C1705632 | lld:lifeskim |
| pubmed-article:15711939 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:15711939 | lifeskim:mentions | umls-concept:C2349975 | lld:lifeskim |
| pubmed-article:15711939 | lifeskim:mentions | umls-concept:C0332291 | lld:lifeskim |
| pubmed-article:15711939 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:15711939 | pubmed:dateCreated | 2005-2-15 | lld:pubmed |
| pubmed-article:15711939 | pubmed:abstractText | Patients with malignant gliomas have a poor prognosis and new treatment paradigms are needed against this disease. TRAIL/Apo2L selectively induces apoptosis in malignant cells sparing normal cells and is hence of interest as a potential therapeutic agent against gliomas. To determine the factors that modulate sensitivity to TRAIL, we examined the differences in TRAIL-activated signaling pathways in glioma cells with variable sensitivities to the agent. Apoptosis in response to TRAIL was unrelated to DR5 expression or endogenous p53 status in a panel of 8 glioma cell lines. TRAIL activated the extrinsic (cleavage of caspase-8, caspase-3 and PARP) and mitochondrial apoptotic pathways and reduced FLIP levels. It also induced caspase-dependent JNK activation, which did not influence TRAIL-induced apoptosis. Because the pro-survival PI3K/Akt pathway is highly relevant to gliomas, we assessed whether Akt could protect against TRAIL-induced apoptosis. Pretreatment with SH-6, a novel Akt inhibitor, enhanced TRAIL-induced apoptosis, suggesting a protective role for Akt. Conversely, TRAIL induced caspase-dependent cleavage of Akt neutralizing its anti-apoptotic effects. These results demonstrate that TRAIL-induced apoptosis in gliomas involves both activation of death pathways and downregulation of survival pathways. Additional studies are warranted to determine the therapeutic potential of TRAIL against gliomas. | lld:pubmed |
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| pubmed-article:15711939 | pubmed:language | eng | lld:pubmed |
| pubmed-article:15711939 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15711939 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:15711939 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:15711939 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15711939 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:15711939 | pubmed:issn | 1360-8185 | lld:pubmed |
| pubmed-article:15711939 | pubmed:author | pubmed-author:BrunerJ MJM | lld:pubmed |
| pubmed-article:15711939 | pubmed:author | pubmed-author:GuoH FHF | lld:pubmed |
| pubmed-article:15711939 | pubmed:author | pubmed-author:KyritsisA PAP | lld:pubmed |
| pubmed-article:15711939 | pubmed:author | pubmed-author:SampathDD | lld:pubmed |
| pubmed-article:15711939 | pubmed:author | pubmed-author:PuduvalliV... | lld:pubmed |
| pubmed-article:15711939 | pubmed:author | pubmed-author:NangiaJJ | lld:pubmed |
| pubmed-article:15711939 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15711939 | pubmed:volume | 10 | lld:pubmed |
| pubmed-article:15711939 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15711939 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15711939 | pubmed:pagination | 233-43 | lld:pubmed |
| pubmed-article:15711939 | pubmed:dateRevised | 2011-9-22 | lld:pubmed |
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| pubmed-article:15711939 | pubmed:meshHeading | pubmed-meshheading:15711939... | lld:pubmed |
| pubmed-article:15711939 | pubmed:year | 2005 | lld:pubmed |
| pubmed-article:15711939 | pubmed:articleTitle | TRAIL-induced apoptosis in gliomas is enhanced by Akt-inhibition and is independent of JNK activation. | lld:pubmed |
| pubmed-article:15711939 | pubmed:affiliation | Department of Neuro-Oncology, The University of Texas M. D. Anderson Cancer Center, Houston, TX 7700, USA. vpuduval@mdanderson.org | lld:pubmed |
| pubmed-article:15711939 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:15711939 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:15711939 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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