车站3
STAT蛋白
贾纳斯激酶
生物
癌症研究
转录因子
个人识别码1
小RNA
细胞生物学
癌症
信号转导
斯达
JAK-STAT信号通路
酪氨酸激酶
磷酸化
遗传学
基因
丝氨酸
作者
Hua Yu,Heehyoung Lee,Andreas Herrmann,Ralf Buettner,Richard Jove
出处
期刊:Nature Reviews Cancer
[Springer Nature]
日期:2014-10-24
卷期号:14 (11): 736-746
被引量:1660
摘要
The Janus kinases (JAKs) and signal transducer and activator of transcription (STAT) proteins, particularly STAT3, are among the most promising new targets for cancer therapy. In addition to interleukin-6 (IL-6) and its family members, multiple pathways, including G-protein-coupled receptors (GPCRs), Toll-like receptors (TLRs) and microRNAs were recently identified to regulate JAK-STAT signalling in cancer. Well known for its role in tumour cell proliferation, survival, invasion and immunosuppression, JAK-STAT3 signalling also promotes cancer through inflammation, obesity, stem cells and the pre-metastatic niche. In addition to its established role as a transcription factor in cancer, STAT3 regulates mitochondrion functions, as well as gene expression through epigenetic mechanisms. Newly identified regulators and functions of JAK-STAT3 in tumours are important targets for potential therapeutic strategies in the treatment of cancer.
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