Institute of Physiological Chemistry, University of Ulm, Ulm, Germany.
J Clin Invest. 2011 Jul;121(7):2551-3. doi: 10.1172/JCI58454. Epub 2011 Jun 23.
Chronic inflammation has long been suspected to support tumorigenesis in a variety of cancers. The IκB kinase (IKK)/NF-κB pathway is the critical signal transduction pathway regulating inflammation, and loss-of-function studies have demonstrated its involvement in tumorigenesis. In this issue of the JCI, Vlantis et al. present evidence that persistent genetic activation of IKK/NF-κB signaling in intestinal epithelial cells not only accelerates tumorigenesis in models of both carcinogen- and mutation-induced colorectal cancer, but also is sufficient to induce intestinal tumors.
慢性炎症长期以来一直被怀疑在多种癌症中支持肿瘤发生。IKK/NF-κB 通路是调节炎症的关键信号转导通路，失活功能研究表明其参与了肿瘤发生。在本期 JCI 中，Vlantis 等人提供了证据，表明在肠道上皮细胞中持续的 IKK/NF-κB 信号的遗传激活不仅加速了化学诱发性和突变诱导的结直肠癌模型中的肿瘤发生，而且足以诱导肠道肿瘤。
