Regis Gabriella, Pensa Sara, Boselli Daniela, Novelli Francesco, Poli Valeria
Molecular Biotechnology Center, University of Turin, via Nizza 52, 10126 Turin, Italy.
Semin Cell Dev Biol. 2008 Aug;19(4):351-9. doi: 10.1016/j.semcdb.2008.06.004. Epub 2008 Jun 22.
Downstream of cytokine or growth factor receptors, STAT3 counteracts inflammation and promotes cell survival/proliferation and immune tolerance while STAT1 inhibits proliferation and favours innate and adaptive immune responses. STAT1 and STAT3 activation are 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 STAT1/3 activation and discuss the hypothesis that perturbation of their expression and/or activation levels may provide novel therapeutic strategies in different clinical settings and particularly in cancer.
在细胞因子或生长因子受体的下游,信号转导和转录激活因子3(STAT3)可对抗炎症,促进细胞存活/增殖和免疫耐受,而信号转导和转录激活因子1(STAT1)则抑制增殖,并有利于先天性和适应性免疫反应。STAT1和STAT3的激活相互调节,其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。在这里,我们综述了STAT1/3激活的功能性经典和非经典效应,并讨论了这样一种假说,即它们的表达和/或激活水平的扰动可能为不同临床环境,特别是癌症提供新的治疗策略。