Journal article
STAT3 and epithelial–mesenchymal transitions in carcinomas
JAK-STAT, Vol.3(2), pp.e28975-e28975
05/01/2014
DOI: 10.4161/jkst.28975
PMCID: PMC4024059
PMID: 24843831
Abstract
Cellular programs coupled to cycles of epithelial–mesenchymal transitions (EMTs) play critical roles during embryogenesis, as well as during tissue development, remodeling, and repair. Research over the last decade has established the importance of an ever-expanding list of master EMT transcription factors, whose activity is regulated by STAT3 and function to stimulate the rapid transition of cells between epithelial and mesenchymal phenotypes. Importantly, inappropriate reactivation of embryonic EMT programs in carcinoma cells underlies their metastasis to distant organ sites, as well as their acquisition of stem cell-like and chemoresistant phenotypes operant in eliciting disease recurrence. Thus, targeted inactivation of master EMT transcription factors may offer new inroads to alleviate metastatic disease. Here we review the molecular, cellular, and microenvironmental factors that contribute to the pathophysiological activities of STAT3 during its regulation of EMT programs in human carcinomas.
Details
- Title: Subtitle
- STAT3 and epithelial–mesenchymal transitions in carcinomas
- Creators
- Michael K Wendt - Purdue University SystemNikolas Balanis - Case Western Reserve UniversityCathleen R Carlin - Case Western Reserve UniversityWilliam P Schiemann - Case Western Reserve University
- Resource Type
- Journal article
- Publication Details
- JAK-STAT, Vol.3(2), pp.e28975-e28975
- Publisher
- Landes Bioscience
- DOI
- 10.4161/jkst.28975
- PMID
- 24843831
- PMCID
- PMC4024059
- ISSN
- 2162-3988
- eISSN
- 2162-3996
- Language
- English
- Date published
- 05/01/2014
- Academic Unit
- Internal Medicine
- Record Identifier
- 9984479360802771
Metrics
6 Record Views