Please use this identifier to cite or link to this item:
Title: Therapeutically exploiting STAT3 activity in cancer - using tissue repair as a road map.
Austin Authors: Huynh, Jennifer;Chand, Ashwini;Gough, Daniel;Ernst, Matthias 
Affiliation: School of Cancer Medicine, La Trobe University, Melbourne, Victoria, Australia
Olivia Newton-John Cancer Research Institute, Heidelberg, Victoria, Australia
Centre for Cancer Research, Hudson Institute of Medical Research, Clayton, Victoria, Australia
Department of Molecular and Translational Science, Monash University, Clayton, Victoria, Australia
Issue Date: 2019 2018-12-21
Publication information: Nature reviews. Cancer 2019; 19(2): 82-96
Abstract: The tightly orchestrated temporal and spatial control of signal transducer and activator of transcription 3 (STAT3) activity in epithelial, immune and stromal cells is critical for wound healing and tissue repair. Excessive STAT3 activation within cancer cells and cells of the tumour microenvironment can be viewed as a neoplastic mimic of an inflammation-driven repair response that collectively promotes tumour progression. In addition to the canonical transcriptional pathways by which STAT3 promotes stem cell-like characteristics, survival, proliferation, metastatic potential and immune evasion, cytoplasmic STAT3 activity fuels tumour growth by metabolic and other non-transcriptional mechanisms. Here, we review the tumour-modulating activities of STAT3 in light of its role as a signalling node integrating inflammatory responses during wound healing. Accordingly, many of the cytokines that contribute to the para-inflammatory state of most solid malignancies converge on and underpin dysregulated STAT3 activity. Targeting of these cytokines, their cognate receptors and associated signalling cascades in clinical trials is beginning to demonstrate therapeutic efficacy, given that interference with STAT3 activity is likely to simultaneously curb the growth of cancer cells and augment antitumour immunity.
DOI: 10.1038/s41568-018-0090-8
ORCID: 0000-0002-2638-8352
PubMed URL: 30578415
Type: Journal Article
Appears in Collections:Journal articles

Show full item record

Page view(s)

checked on Dec 9, 2022

Google ScholarTM


Items in AHRO are protected by copyright, with all rights reserved, unless otherwise indicated.