ArticleThe Journal of pharmacology and experimental therapeutics2026
Aryl hydrocarbon receptor as a molecular mediator in the induction of human aldehyde oxidase gene expression.
Article in The Journal of pharmacology and experimental therapeutics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Relatively little is known about receptor-mediated regulation of aldehyde oxidase (AOX). 2,3,7,8-Tetrachlorodibenzo-p-dioxin, an aryl hydrocarbon receptor (AHR) agonist, increases mouse Aox expression. However, given the species differences in ligand-dependent AHR activation and AOX regulation, it remains to be investigated whether human AHR regulates the expression of AOX1 (the human AOX isoform). Therefore, the present study was designed to determine the effect of modulating the functionality of human AHR on AOX1 gene expression in cell culture models (HepG2 and MCF-7) known to express AHR and AOX1. Treatment of HepG2 or MCF-7 cells with a noncytotoxic concentration of a classical AHR agonist (β-naphthoflavone, benzo[a]pyrene, or 3-methylcholanthrene [3-MC]), an endogenous AHR agonist (indoxyl sulfate or 6-formylindolo[3,2-b]carbazole), or a selective AHR modulator (quercetin, 3,3'-diindolylmethane, or omeprazole) increased AOX1 and AHR-regulated CYP1A1 mRNA expression. The increases in AOX1 and CYP1A1 mRNA levels were not correlated among our panel of AHR activators. The induction of AOX1 mRNA by 3-MC was time- and concentration-dependent. It was accompanied by an increase in AOX1 protein expression and AOX1-mediated enzyme activity (O
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