Avalle Lidia, Pensa Sara, Regis Gabriella, Novelli Francesco, Poli Valeria
Molecular Biotechnology Center and Department of Genetics, Biology and Biochemistry; University of Turin; Turin, Italy.
JAKSTAT. 2012 Apr 1;1(2):65-72. doi: 10.4161/jkst.20045.
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.
转录因子STAT1和STAT3在肿瘤发生过程中似乎发挥着相反的作用。虽然STAT3促进细胞存活/增殖、迁移和免疫耐受,被视为一种癌基因,但STAT1大多触发抗增殖和促凋亡反应,同时增强抗肿瘤免疫力。尽管它们在常见细胞因子和生长因子受体的下游被激活,但其激活受到相互调节,平衡表达或磷酸化水平的扰动可能会将细胞因子/生长因子信号从增殖导向凋亡,或从炎症导向抗炎。在此,我们综述了STAT1和STAT3激活在肿瘤发生中的功能性经典和非经典效应及其潜在的交叉调节机制。