Please use this identifier to cite or link to this item: http://ahro.austin.org.au/austinjspui/handle/1/20036
Title: Therapeutically exploiting STAT3 activity in cancer - using tissue repair as a road map.
Authors: Huynh, Jennifer;Chand, Ashwini;Gough, Daniel;Ernst, Matthias
Affiliation: 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
School of Cancer Medicine, La Trobe University, Melbourne, Victoria, Australia
Issue Date: 21-Dec-2018
EDate: 2018-12-21
Citation: Nature reviews. Cancer 2018; online first: 21 December
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.
URI: http://ahro.austin.org.au/austinjspui/handle/1/20036
DOI: 10.1038/s41568-018-0090-8
ORCID: 0000-0002-2638-8352
0000-0002-1245-729X
0000-0001-6479-1735
0000-0002-6399-1177
PubMed URL: 30578415
Type: Journal Article
Review
Appears in Collections:Journal articles

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