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The role of NF-κB in the pathogenesis of glioma
Vineshkumar Thidil Puliyappadamba1, Kimmo J Hatanpaa2, Sharmistha Chakraborty3
1Department of Neurology and Neurotherapeutics; University of Texas Southwestern Medical Center, Dallas, TX 75235; Current address: Department of Radiation Oncology, University of Alabama, Birmingham, Birmingham, AL 35294.
Abstract:
Activation of NF-κB affects multiple aspects of cancer biology including cell survival and resistance to treatment. Glioblastoma (GBM) is the most common primary malignant tumor of the brain in adults and is resistant to treatment. Recent studies have reported that NF-κB activation in GBM is widespread and have elucidated the underlying regulatory mechanisms. EGFR gene amplification and mutation are among the key genetic alterations in GBM, and aberrant EGFR signaling is a key activator of NF-κB in GBM. In this review we discuss the evidence for activation of NF-κB in GBM and the key signaling pathways involved. Substantial evidence suggests a role for NF-κB in the pathogenesis of GBM and its resistance to treatment, indicating that NF-κB pathways may be useful targets for treatment.
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