Xiao Gutian, Fu Jing
University of Pittsburgh Cancer Institute, Department of Microbiology and Molecular Genetics, University of Pittsburgh School of Medicine Pittsburgh, Pennsylvania 15213, USA.
Am J Cancer Res. 2011;1(2):192-221. Epub 2010 Dec 6.
Recent studies have clearly linked nuclear factor-kappaB (NF-κB), a transcription factor that plays a central role in regulating immune and inflammatory responses, to tumor development, progression, and metastasis as well as tumor therapy resistance. However, it still remains largely unknown on how the tightly regulated NF-κB becomes constitutively activated in tumorigenesis and how the original cancer immunosurveillance function of NF-κB is transformed to be tumorigenic. To address these important issues for cancer prevention and treatment, we discuss current understanding of the molecular mechanisms and molecules involved in the oncogenic activation of NF-κB. We also discuss current understanding of how NF-κB coordinates the inflammatory and malignant cells in tumorigenesis.
近期研究已明确将核因子-κB（NF-κB）——一种在调节免疫和炎症反应中起核心作用的转录因子——与肿瘤发生、发展、转移以及肿瘤治疗耐药性联系起来。然而，在肿瘤发生过程中受到严格调控的NF-κB是如何持续激活的，以及NF-κB最初的癌症免疫监视功能是如何转变为致瘤功能的，目前仍 largely未知。为了解决这些癌症预防和治疗的重要问题，我们讨论了目前对NF-κB致癌激活所涉及的分子机制和分子的理解。我们还讨论了目前对NF-κB在肿瘤发生过程中如何协调炎症细胞和恶性细胞的理解。
