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.File | Dimensione | Formato | |
---|---|---|---|
Avalle L, Pensa et al._4aperto.pdf
file disponibile solo agli amministratori
Licenza:
DRM non definito
Dimensione
3.76 MB
Formato
Adobe PDF
|
3.76 MB | Adobe PDF | Visualizza/Apri Richiedi una copia |
I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.