NF-κB and STAT3 signaling in glioma: targets for future therapies

Abstract

Glioblastoma remains the most clinically challenging tumor of the CNS, as evidenced by the dismal change in overall survival over the past 50 years. However, recent advances in high-throughput screening techniques have given rise to a wealth of new information regarding the aberrant signaling pathways that drive the tumor phenotype. Two of these so-called ‘oncopathways’ are NF-κB and JAK/STAT. This review will describe the basic mechanisms of these pathways, explore the relevance of NF-κB and JAK/STAT signaling in glioblastoma, and look ahead to experimental compounds that will integrate our knowledge of these pathways into existing therapies.

Keywords::

• cytokine
• glioblastoma
• intracellular signaling
• JAK/STAT
• NF-κB

Acknowledgements

The authors would like to thank to Brandi Baker (UAB) for reading the manuscript.

Financial & competing interests disclosure

This work was supported in part by National Institutes of Health grants CA-97247 (ENB), NS-50665 (ENB), IRG-60-001-47 from the American Cancer Society and CA-13148-31 from the NCI (SEN), NIH CA-13148-35 (ENB), P30 CA-13149-38 from the UAB Comprehensive Cancer Center (ENB), and the Southeastern Brain Tumor Foundation (SEN). George P Atkinson was supported by the UAB Medical Scientist Training Program and by NIH T32-AI0705. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.