Molecular Pathways: Dietary Regulation of Stemness and Tumor Initiation by the PPAR- Pathway
Name
nihms827156.pdf
Size
626.71 KB
Format
Adobe PDF
Checksum (MD5)
741e34c6e5e30322baf95426467b80f2
Author(s)
Beyaz, Semir
Yilmaz, Omer
Date Issued
October 2016
Journal
Clinical Cancer Research
Publisher
American Association for Cancer Research (AACR)
Citation
Beyaz, S. and O. H. Yilmaz. “Molecular Pathways: Dietary Regulation of Stemness and Tumor Initiation by the PPAR- Pathway.” Clinical Cancer Research 22, 23 (October 2016): 5636–5641 © 2016 American Association for Cancer Research
Version
Author's final manuscript
Abstract
Peroxisome proliferator-activated receptor delta (PPAR-8) is a nuclear receptor transcription factor that regulates gene expression during development and disease states, such as cancer. However, the precise role of PPAR-8 during tumorigenesis is not well understood. Recent data suggest that PPAR-8 may have context-specific oncogenic and tumor-suppressive roles depending on the tissue, cell-type, or diet-induced physiology in question. For example, in the intestine, pro-obesity diets, such as a high-fat diet (HFD), are associated with increased colorectal cancer incidence. Interestingly, many of the effects of an HFD in the stem and progenitor cell compartment are driven by a robust PPAR-8 program and contribute to the early steps of intestinal tumorigenesis. Importantly, the PPAR-8 pathway or its downstream mediators may serve as therapeutic intervention points or biomarkers in colon cancer that arise in patients who are obese. Although potent PPAR-8 agonists and antagonists exist, their clinical utility may be enhanced by uncovering how PPAR-8 mediates tumorigenesis in diverse tissues and cell types as well as in response to diet.
MIT Department
Koch Institute for Integrative Cancer Research at MIT
Terms of Use
Creative Commons Attribution-Noncommercial-Share Alike
Persistent DSpace Link
DOI of Published Version
https://doi.org/10.1158/1078-0432.CCR-16-0775
