Puliyappadamba Vineshkumar Thidil, Hatanpaa Kimmo J, Chakraborty Sharmistha, Habib Amyn A
Department 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.
Pathology at the University of Texas Southwestern Medical Center ; Dallas TX 75390.
Mol Cell Oncol. 2014 Dec 23;1(3):e963478. doi: 10.4161/23723548.2014.963478. eCollection 2014 Jul-Sep.
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.
核因子κB（NF-κB）的激活影响癌症生物学的多个方面，包括细胞存活和对治疗的抗性。胶质母细胞瘤（GBM）是成人中最常见的原发性脑恶性肿瘤，且对治疗具有抗性。最近的研究报道，GBM中NF-κB的激活很普遍，并阐明了其潜在的调控机制。表皮生长因子受体（EGFR）基因扩增和突变是GBM中的关键基因改变，异常的EGFR信号传导是GBM中NF-κB的关键激活剂。在本综述中，我们讨论了GBM中NF-κB激活的证据以及相关的关键信号通路。大量证据表明NF-κB在GBM的发病机制及其对治疗的抗性中起作用，这表明NF-κB信号通路可能是治疗的有用靶点。
