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.
| Original language | English |
|---|---|
| Pages (from-to) | 65-72 |
| Number of pages | 8 |
| Journal | JAK-STAT |
| Volume | 1 |
| DOIs | |
| Publication status | Published - 2012 |
Keywords
- STAT1
- STAT3
- tumorigenesis
- oncogene
- tumor suppressor
- inflammation
- apoptosis
- proliferation
- survival
- metastasis
- tumor invasivity
- anti-tumor immune response
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