Molecular pathways: IL11 as a tumor-promoting cytokine-translational implications for cancers
- Author(s)
- Ernst, M; Putoczki, TL;
- Details
- Publication Year 2014-07-29,Volume 20,Issue #22,Page 5579-5588
- Journal Title
- Clinical Cancer Research
- Publication Type
- Journal Article
- Abstract
- Emerging evidence suggests that cytokines produced by inflammatory cells act as rheostats to link the degree of wounding and local inflammation to epithelial cell survival, proliferation, and metabolism that collectively underpin the repair response. Among these cytokines, the GP130 family, which encompasses among others interleukin (IL)-6 and -11, plays a major role in orchestrating these complex processes through the activation of the latent signal transducer and activator of transcription 3 (STAT3) in the epithelium. However, many of the molecular mechanisms that govern and ensure effective epithelial wound healing and regeneration renewal also promote tumorigenesis and the progression of established cancers. Accordingly, GP130 cytokines endow the inflammatory tumor microenvironment with a capacity to promote "cancer hallmark capabilities" of the malignant epithelium, while simultaneously suppressing the anti-tumor response of innate and adaptive immune cells. Here, we review some recent insights derived from genetic and therapeutic inhibition of the IL6/IL11 - GP130 - STAT3 signalling cascade in the context of preclinical mouse models of cancer, which are likely to have implications to other solid malignancies.
- Publisher
- AACR
- Research Division(s)
- Cell Signalling And Cell Death; Inflammation
- Publisher's Version
- https://doi.org/10.1158/1078-0432.ccr-13-2492
- NHMRC Grants
- NHMRC/1008614, NHMRC/487922, NHMRC/433617, NHMRC/603122,
- Terms of Use/Rights Notice
- ©2014 American Association for Cancer Research
Creation Date: 2014-09-12 02:01:40
Last Modified: 2020-04-07 02:24:01