STATs in cancer inflammation and immunity: a leading role for STAT3.

STATs in cancer inflammation and immunity: a leading role for STAT3.
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DOI:
10.1038/nrc2734
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发表时间:
2009-11
期刊:
Nature reviews. Cancer
影响因子:
--
通讯作者:
Jove R
Jove R
中科院分区:
其他
文献类型:
--
作者:
Yu H;Pardoll D;Jove R

文献摘要

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与其在调节细胞因子依赖性炎症和免疫中的作用相称,信号换能器和转录激活因子(STAT)蛋白在决定肿瘤微环境中的免疫反应是促进还是抑制癌症方面发挥着核心作用。STAT3和STAT5的持续激活在一定程度上增加肿瘤细胞的增殖、存活和侵袭,同时抑制抗肿瘤免疫。STAT3的持续激活也介导促肿瘤炎症。STAT3在肿瘤炎症和免疫中具有双重作用,通过促进促癌炎症途径,包括核因子-κ b (NF-κ b)和白细胞介素-6 (IL-6) - gp130 - janus激酶(JAK)途径,并通过对抗STAT1-和NF-κ b介导的T辅助1抗肿瘤免疫反应。因此,STAT3是一个很有希望的靶点,可以重新定向炎症以用于癌症治疗。
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-κB (NF-κB) and interleukin-6 (IL-6)–GP130–Janus kinase (JAK) pathways, and by opposing STAT1- and NF-κB-mediated T helper 1 anti-tumour immune responses. Consequently, STAT3 is a promising target to redirect inflammation for cancer therapy.