The Role of Peroxisome Proliferator-Activated Receptors in the Esophageal, Gastric, and Colorectal Cancer

<table>PPARs-mediated mechanisms of transcriptional regulation. In the absence of ligands, PPARs bind the promoters of their target genes and repress transcription by recruiting the corepressor complex. In the presence of ligands, PPARs can induce either ligand-dependent transactivation or transrepression. Transactivation involves PPARs heterodimerization with the retinoid X receptors (RXRs) followed by recognition of specific PPAR response elements (PPREs) and interaction with coactivators. Transrepression involves interference with other signal transduction pathways, including <svg height="10.6375" id="M1" style="vertical-align:-0.13792pt" version="1.1" viewbox="0 0 29.387501 10.6375" width="29.387501" xmlns="http://www.w3.org/2000/svg">
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<tspan style="font-size: 12.50px; " x="0" y="0">N</tspan>
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</svg>B, STAT, and AP1. <svg height="10.6375" id="M2" style="vertical-align:-0.13792pt" version="1.1" viewbox="0 0 29.387501 10.6375" width="29.387501" xmlns="http://www.w3.org/2000/svg">
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</svg>B-RE: <svg height="10.6375" id="M3" style="vertical-align:-0.13792pt" version="1.1" viewbox="0 0 29.387501 10.6375" width="29.387501" xmlns="http://www.w3.org/2000/svg">
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</svg>B response element; IFN-RE = “interferon-stimulated gene factor” responsive element; TRE = O-tetradecanoylphorbol 13-acetate-responsive element.</table>

PPAR Research

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Figure 1

Figure 1: The Role of Peroxisome Proliferator-Activated Receptors in the Esophageal, Gastric, and Colorectal Cancer 