Li Qiutang, Withoff Sebo, Verma Inder M
Laboratory of Genetics, The Salk Institute for Biological Studies, La Jolla, CA 92037, USA.
Trends Immunol. 2005 Jun;26(6):318-25. doi: 10.1016/j.it.2005.04.003.
It has long been suspected that NF-kappaB signaling has a pivotal role in chronic inflammation-associated malignancies, although genetic evidence for this hypothesis has been lacking. However, recent papers have lent credence to this concept and show that NF-kappaB activation in pre-malignant cells contributes to cell survival and metastatic potential. Furthermore, NF-kappaB activation in tumor-associated leukocytes, especially macrophages, contributes towards tumorigenesis by upregulating tumor-promoting proinflammatory proteins. This emphasizes the importance of NF-kappaB inhibitors as immunotherapeutic agents for chronic inflammation and suggests that these reagents might prevent, or at least inhibit, chronic inflammation-associated tumorigenesis.
长期以来，人们一直怀疑核因子-κB信号传导在慢性炎症相关的恶性肿瘤中起关键作用，尽管这一假说缺乏遗传学证据。然而，最近的论文证实了这一观点，并表明癌前细胞中的核因子-κB激活有助于细胞存活和转移潜能。此外，肿瘤相关白细胞尤其是巨噬细胞中的核因子-κB激活通过上调促进肿瘤的促炎蛋白促进肿瘤发生。这强调了核因子-κB抑制剂作为慢性炎症免疫治疗药物的重要性，并表明这些试剂可能预防或至少抑制慢性炎症相关的肿瘤发生。
