NDLI: Tumor Necrosis Factor-Like Weak Inducer of Apoptosis (TWEAK) Stimulation of Glioma Cell Survival Is Dependent Upon Akt2 Function

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Tumor Necrosis Factor-Like Weak Inducer of Apoptosis (TWEAK) Stimulation of Glioma Cell Survival Is Dependent Upon Akt2 Function

Content Provider	PubMed Central
Author	Fortin, Shannon P. Ennis, Matthew J. Savitch, Benjamin A. Carpentieri, David Mcdonough, Wendy S. Winkles, Jeffrey A. Loftus, Joseph C. Kingsley, Christopher Hostetter, Galen Tran, Nhan L.
Abstract	Malignant gliomas are the most common primary brain tumors. Despite intensive clinical investigation and significant technical advances in surgical and radiation treatment, the impact on clinical outcome for patients with malignant gliomas is disappointing. We have previously shown that TWEAK, a member of the TNF superfamily, can stimulate glioma cell survival via binding to the Fn14 receptor, activation of the NF-κB pathway, and up-regulation of BCL-XL gene expression. Here, we show that TWEAK treatment of glioma cells leads to phosphorylation of Akt and BAD. TWEAK stimulation results in the phosphorylation of both Akt1 and Akt2. However, siRNA-mediated depletion of either Akt1 or Akt2 showed that BAD serine 136 phosphorylation is dependent specifically on Akt2 function. Depletion of Akt2 expression by siRNA also abrogates TWEAK-stimulated glioma cell survival, whereas no effect on glioma cell survival was observed after siRNA-mediated depletion of Akt1 expression. Surprisingly, although siRNA-mediated depletion of BAD in glioma cells abrogates cytotoxic- and chemotherapy-induced apoptosis, TWEAK still display a strong protective effect, suggesting that BAD serine 136 phosphorylation plays a minor role in TWEAK-Akt2 induced glioma cells survival. We also report here that AKT2 gene expression levels increased with glioma grade and inversely correlate with patient survival. Additionally, immunohistochemical analysis showed that Akt2 expression positively correlates with Fn14 expression in GBM specimens. We hypothesize that the TWEAK-Fn14 signaling axis functions, in part, to enhance glioblastoma cell survival by activation of the Akt2 serine/threonine protein kinase.
Related Links	http://dx.doi.org/10.1158/1541-7786.mcr-09-0194
Ending Page	1881
Page Count	11
Starting Page	1871
File Format	PDF
ISSN	15417786
e-ISSN	15573125
Journal	Molecular cancer research : MCR
Issue Number	11
Volume Number	7
Language	English
Publisher Date	2009-11-01
Access Restriction	Open
Subject Keyword	Cancer Research Oncology Molecular Biology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Molecular Biology Cancer Research Oncology

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