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核因子-κB与癌症:机制与靶点

NF-kappaB and cancer: mechanisms and targets.

作者信息

Karin Michael

机构信息

Laboratory of Gene Regulation and Signal Transduction, Department of Pharmacology, University of California San Diego, School of Medicine, La Jolla, California 92093, USA.

出版信息

Mol Carcinog. 2006 Jun;45(6):355-61. doi: 10.1002/mc.20217.

DOI:10.1002/mc.20217
PMID:16673382
Abstract

In addition to being a central coordinator of immune responses, NF-kappaB signaling also plays a critical role in cancer development and progression and it may determine the response to therapy. NF-kappaB activation was shown to provide a critical mechanistic link between inflammation and cancer and is a major factor that controls the ability of both preneoplastic and malignant cells to resist apoptosis-based tumor surveillance mechanisms. NF-kappaB may also be involved in regulation of tumor angiogenesis and invasiveness. Importantly, NF-kappaB and the signaling pathways that mediate its activation have become attractive targets for development of new chemopreventive and chemotherapeutic approaches.

摘要

除了作为免疫反应的中央协调器外,核因子κB信号传导在癌症的发生和发展中也起着关键作用,并且可能决定对治疗的反应。核因子κB的激活被证明在炎症与癌症之间提供了关键的机制联系,并且是控制癌前细胞和恶性细胞抵抗基于凋亡的肿瘤监测机制能力的主要因素。核因子κB也可能参与肿瘤血管生成和侵袭的调节。重要的是,核因子κB及其介导激活的信号通路已成为开发新的化学预防和化疗方法的有吸引力的靶点。

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