车站3
STAT蛋白
癌症研究
免疫系统
间质细胞
生物
癌细胞
伤口愈合
炎症
癌症
信号转导
肿瘤微环境
细胞生物学
免疫学
遗传学
作者
Jennifer Huynh,Ashwini L. Chand,Daniel J. Gough,Matthias Ernst
出处
期刊:Nature Reviews Cancer
[Springer Nature]
日期:2018-12-21
卷期号:19 (2): 82-96
被引量:340
标识
DOI:10.1038/s41568-018-0090-8
摘要
The tightly orchestrated temporal and spatial control of signal transducer and activator of transcription 3 (STAT3) activity in epithelial, immune and stromal cells is critical for wound healing and tissue repair. Excessive STAT3 activation within cancer cells and cells of the tumour microenvironment can be viewed as a neoplastic mimic of an inflammation-driven repair response that collectively promotes tumour progression. In addition to the canonical transcriptional pathways by which STAT3 promotes stem cell-like characteristics, survival, proliferation, metastatic potential and immune evasion, cytoplasmic STAT3 activity fuels tumour growth by metabolic and other non-transcriptional mechanisms. Here, we review the tumour-modulating activities of STAT3 in light of its role as a signalling node integrating inflammatory responses during wound healing. Accordingly, many of the cytokines that contribute to the para-inflammatory state of most solid malignancies converge on and underpin dysregulated STAT3 activity. Targeting of these cytokines, their cognate receptors and associated signalling cascades in clinical trials is beginning to demonstrate therapeutic efficacy, given that interference with STAT3 activity is likely to simultaneously curb the growth of cancer cells and augment antitumour immunity. This Review discusses how excessive signal transducer and activator of transcription 3 (STAT3) activation within cancer cells and cells of the tumour microenvironment can be viewed as a neoplastic mimic of an inflammation-driven repair response that promotes tumour progression.
科研通智能强力驱动
Strongly Powered by AbleSci AI