Laboratory of Gene Regulation and Signal Transduction, Departments of Pharmacology and Pathology, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA; Moores Cancer Center, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA.
Cancer Cell. 2014 Oct 13;26(4):447-9. doi: 10.1016/j.ccell.2014.09.012.
NF-κB protects malignant cells from death and therefore it was considered as a cancer treatment target. However, systemic NF-κB inhibition resulted in inflammation and other undesired outcomes. In this issue of Cancer Cell, Tornatore and colleagues solve this problem by targeting the GADD45:MKK7 module mediating NF-κB-induced survival of multiple myelomas.
NF-κB 可保护恶性细胞免于死亡，因此被视为癌症治疗的靶点。然而，全身性 NF-κB 抑制会导致炎症和其他不良后果。在本期《癌细胞》杂志中，Tornatore 及其同事通过靶向介导 NF-κB 诱导多发性骨髓瘤细胞存活的 GADD45:MKK7 模块解决了这个问题。
