TRAIL-induced apoptosis in gliomas is enhanced by Akt-inhibition and is independent of JNK activation View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2005-01

AUTHORS

V. K. Puduvalli, D. Sampath, J. M. Bruner, J. Nangia, R. Xu, A. P. Kyritsis

ABSTRACT

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. More... »

PAGES

233-243

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s10495-005-6078-3

DOI

http://dx.doi.org/10.1007/s10495-005-6078-3

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1046921353

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/15711939


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