Department of Biochemistry and Medical Biotechnology, University of Naples Federico II, Via Pansini, 5, 80131 Naples, Italy.
Curr Opin Pharmacol. 2011 Aug;11(4):288-93. doi: 10.1016/j.coph.2011.04.011. Epub 2011 May 11.
Constitutive activation of NF-κB occurs in a significant percentage of human cancers. Genetic abnormalities of tumors often enhance normal NF-κB signaling. Chronic inflammation is also associated with constitutive NF-κB activation and increases the risk of cancer. Aberrant NF-κB activation favors cellular transformation, sustains cancer survival, and contributes to tumor invasion. Strategies to inhibit NF-κB represent a promising therapeutic option against cancer. In the last decade, several studies point to the large immunophilin FKBP51 as an important element for the control of NF-κB activation in human neoplasia. This article is an overview of the causes of aberrant NF-κB regulation in cancer and highlights recent papers that implicate FKBP51 in such deregulation.
NF-κB 的组成性激活发生在很大比例的人类癌症中。肿瘤的遗传异常通常会增强正常的 NF-κB 信号。慢性炎症也与组成性 NF-κB 激活有关，并增加癌症的风险。异常的 NF-κB 激活有利于细胞转化，维持癌症的存活，并有助于肿瘤的侵袭。抑制 NF-κB 的策略是对抗癌症的一种很有前途的治疗选择。在过去的十年中，有几项研究指出，大免疫亲和素 FKBP51 是控制人类肿瘤中 NF-κB 激活的重要因素。本文概述了癌症中 NF-κB 调节异常的原因，并强调了最近的一些论文，这些论文表明 FKBP51 在这种失调中起作用。
