ABSTRACT
Abstract he 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 enhances inflammation and innate and adaptive
immunity, triggering in most instances anti-proliferative and pro-apoptotic responses in tumor cells. Despite being activated downstream of common cytokine and growth factor receptors, their activation is reciprocally regulated and perturbation in their balanced expression or phosphoryla tion levels may redirect 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 and discuss the hypothesis that perturbation of their expression and/or activation levels may provide novel cancer therapeutic strategies.
