IKK/NF-κB and STAT3 pathways: central signalling hubs in inflammation-mediated tumour promotion and metastasis

被引:369
作者
Bollrath, Julia [1 ]
Greten, Florian R. [1 ]
机构
[1] Tech Univ Munich, Dept Med 2, Klinikum Rechts Isar, D-81675 Munich, Germany
关键词
inflammation; signal transduction; carcinogenesis; myeloid cells; COLITIS-ASSOCIATED TUMORIGENESIS; CANCER-RELATED INFLAMMATION; COMPENSATORY PROLIFERATION; HEPATOCELLULAR-CARCINOMA; IMMUNE-SYSTEM; MYELOID CELLS; MUTANT MICE; T-CELLS; BETA; MICROENVIRONMENT;
D O I
10.1038/embor.2009.243
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
Our understanding of the molecular mechanisms that link inflammation and cancer has significantly increased in recent years. Here, we analyse genetic evidence indicating that the transcription factors nuclear factor-kappa B (NF-kappa B) and signal transducer and activator of transcription 3 (STAT3) have a central role in this context by regulating distinct functions in cancer cells and surrounding non-tumorigenic cells. In immune cells, NF-kappa B induces the transcription of genes that encode pro-inflammatory cytokines, which can act in a paracrine manner on initiated cells. By contrast, in tumorigenic cells, both NF-kappa B and STAT3 control apoptosis, and STAT3 can also enhance proliferation. Consequently, inflammation should be considered as a valuable target for cancer prevention and therapy.
引用
收藏
页码:1314 / 1319
页数:6
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