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Molecular Pathways: Dietary Regulation of Stemness and Tumor Initiation by the PPAR-? Pathway.


ABSTRACT: Peroxisome proliferator-activated receptor delta (PPAR-?) is a nuclear receptor transcription factor that regulates gene expression during development and disease states, such as cancer. However, the precise role of PPAR-? during tumorigenesis is not well understood. Recent data suggest that PPAR-? 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-? program and contribute to the early steps of intestinal tumorigenesis. Importantly, the PPAR-? 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-? agonists and antagonists exist, their clinical utility may be enhanced by uncovering how PPAR-? mediates tumorigenesis in diverse tissues and cell types as well as in response to diet. Clin Cancer Res; 22(23); 5636-41. ©2016 AACR.

SUBMITTER: Beyaz S 

PROVIDER: S-EPMC5135602 | biostudies-literature | 2016 Dec

REPOSITORIES: biostudies-literature

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Molecular Pathways: Dietary Regulation of Stemness and Tumor Initiation by the PPAR-δ Pathway.

Beyaz Semir S   Yilmaz Ömer H ÖH  

Clinical cancer research : an official journal of the American Association for Cancer Research 20161004 23


Peroxisome proliferator-activated receptor delta (PPAR-δ) is a nuclear receptor transcription factor that regulates gene expression during development and disease states, such as cancer. However, the precise role of PPAR-δ during tumorigenesis is not well understood. Recent data suggest that PPAR-δ 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  ...[more]

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