STAT蛋白
车站3
炎症
STAT1
免疫系统
癌症研究
贾纳斯激酶
生物
免疫
状态5
细胞因子
免疫学
斯达
信号转导
细胞生物学
干扰素
作者
Hua Yu,Drew M. Pardoll,Richard Jove
出处
期刊:Nature Reviews Cancer
[Springer Nature]
日期:2009-11-01
卷期号:9 (11): 798-809
被引量:3520
摘要
Commensurate with their roles in regulating cytokine-dependent inflammation and immunity, signal transducer and activator of transcription (STAT) proteins are central in determining whether immune responses in the tumour microenvironment promote or inhibit cancer. Persistently activated STAT3 and, to some extent, STAT5 increase tumour cell proliferation, survival and invasion while suppressing anti-tumour immunity. The persistent activation of STAT3 also mediates tumour-promoting inflammation. STAT3 has this dual role in tumour inflammation and immunity by promoting pro-oncogenic inflammatory pathways, including nuclear factor-kappaB (NF-kappaB) and interleukin-6 (IL-6)-GP130-Janus kinase (JAK) pathways, and by opposing STAT1- and NF-kappaB-mediated T helper 1 anti-tumour immune responses. Consequently, STAT3 is a promising target to redirect inflammation for cancer therapy.
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