Epigallocatechin Gallate Inhibits Aryl Hydrocarbon Receptor Gene Transcription through an Indirect Mechanism Involving Binding to a 90 kDa Heat Shock Protein
The aryl hydrocarbon receptor (AAhR) is a ligand-activated transcription factor known to mediate the toxic effects of numerous environmental contaminants, including the polycyclic aromatic hydrocarbons (PAHs). Historically, binding of PAHs to the AhR and the events leading to the generation of DNA adducts have been associated with chemical carcinogens. Previous investigations have implicated green tea (GT) as affording protection against PAH-induced cancers in animal models. Investigations in our laboratory have demonstrated that the GT polyphenol epigallocatechin gallate (EGCG) is capable of antagonizing the AhR-mediated gene transcription, implicating the inhibition of AhR signaling as a potential chemopreventative mechanism. Read More.
The aryl hydrocarbon receptor (AAhR) is a ligand-activated transcription factor known to mediate the toxic effects of numerous environmental contaminants, including the polycyclic aromatic hydrocarbons (PAHs). Historically, binding of PAHs to the AhR and the events leading to the generation of DNA adducts have been associated with chemical carcinogens. Previous investigations have implicated green tea (GT) as affording protection against PAH-induced cancers in animal models. Investigations in our laboratory have demonstrated that the GT polyphenol epigallocatechin gallate (EGCG) is capable of antagonizing the AhR-mediated gene transcription, implicating the inhibition of AhR signaling as a potential chemopreventative mechanism. Read More.