Abstract：
:Glial tumors progress to malignant grades by heightened proliferation and relentless dispersion throughout the central nervous system. Understanding genetic and biochemical processes that foster these behaviors is likely to reveal specific and effective targets for therapeutic intervention. Our current report shows that the fibroblast growth factor-inducible 14 (Fn14), a member of the tumor necrosis factor (TNF) receptor superfamily, is expressed at high levels in migrating glioma cells in vitro and invading glioma cells in vivo. Forced Fn14 overexpression stimulates glioma cell migration and invasion, and depletion of Rac1 by small interfering RNA inhibits this cellular response. Activation of Fn14 signaling by the ligand TNF-like weak inducer of apoptosis (TWEAK) stimulates migration and up-regulates expression of Fn14; this TWEAK effect requires Rac1 and nuclear factor-kappaB (NF-kappaB) activity. The Fn14 promoter region contains NF-kappaB binding sites, which mediate positive feedback causing sustained overexpression of Fn14 and enduring glioma cell invasion. Furthermore, Fn14 gene expression levels increase with glioma grade and inversely correlate with patient survival. These results show that the Fn14 cascade operates as a positive feedback mechanism for elevated and sustained Fn14 expression. Such a feedback loop argues for aggressive targeting of the Fn14 axis as a unique and specific driver of glioma malignant behavior.
journal_name
Cancer Resjournal_title
Cancer researchauthors
Tran NL,McDonough WS,Savitch BA,Fortin SP,Winkles JA,Symons M,Nakada M,Cunliffe HE,Hostetter G,Hoelzinger DB,Rennert JL,Michaelson JS,Burkly LC,Lipinski CA,Loftus JC,Mariani L,Berens MEdoi
10.1158/0008-5472.CAN-06-0418subject
Has Abstractpub_date
2006-10-01 00:00:00pages
9535-42issue
19eissn
0008-5472issn
1538-7445pii
66/19/9535journal_volume
66pub_type
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