STAT1 and STAT3 in tumorigenesis: A matter of balance.
STAT1 and STAT3 in tumorigenesis: A matter of balance.
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DOI：
10.4161/jkst.20045
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发表时间：
2012-04-01
期刊：
影响因子：
--
通讯作者：
Poli V
中科院分区：
文献类型：
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作者：
Avalle L;Pensa S;Regis G;Novelli F;Poli V
转录因子STAT 1和STAT 3在肿瘤发生中起着相反的作用。虽然STAT 3促进细胞存活/增殖、运动性和免疫耐受，并且被认为是致癌基因，但STAT 1主要触发抗增殖和促凋亡反应，同时增强抗肿瘤免疫。尽管在常见的细胞因子和生长因子受体的下游被激活，但它们的激活是可调节的，并且它们的平衡表达或磷酸化水平的扰动可以将细胞因子/生长因子信号从增殖重定向到凋亡，或从炎症重定向到抗炎。本文综述了STAT 1和STAT 3在肿瘤发生中的典型和非典型作用及其潜在的交叉调节机制。
The transcription factors STAT1 and STAT3 appear to play opposite roles in tumorigenesis. While STAT3 promotes cell survival/proliferation, motility and immune tolerance and is considered as an oncogene, STAT1 mostly triggers anti-proliferative and pro-apoptotic responses while enhancing anti-tumor immunity. Despite being activated downstream of common cytokine and growth factor receptors, their activation is reciprocally regulated and perturbation in their balanced expression or phosphorylation levels may re-direct cytokine/growth factor signals from proliferative to apoptotic, or from inflammatory to anti-inflammatory. Here we review the functional canonical and non-canonical effects of STAT1 and STAT3 activation in tumorigenesis and their potential cross-regulation mechanisms.