The transcription factors STAT1 and STAT3 appear to play opposite role in tumorigenesis. While STAT3 propmotes survival/proliferation, motility and immune tolerance and is considered as an oncogene, STAT1 mostly triggers antiproliferative 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 crossregulation mechanisms.

STAT1 and STAT3 in tumorigenesis: A matter of balance

AVALLE, LIDIA;
2012-01-01

Abstract

The transcription factors STAT1 and STAT3 appear to play opposite role in tumorigenesis. While STAT3 propmotes survival/proliferation, motility and immune tolerance and is considered as an oncogene, STAT1 mostly triggers antiproliferative 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 crossregulation mechanisms.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11579/171053
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