The search of CAR, AhR, ESRs binding sites in promoters of intronic and intergenic microRNAs

Vladimir Y. Ovchinnikov, Denis V. Antonets, Lyudmila F. Gulyaeva

    Research output: Contribution to journalArticlepeer-review

    6 Citations (Scopus)


    MicroRNAs (miRNAs) play important roles in the regulation of gene expression at the post-transcriptional level. Many exogenous compounds or xenobiotics may affect microRNA expression. It is a well-established fact that xenobiotics with planar structure like TCDD, benzo(a)pyrene (BP) can bind aryl hydrocarbon receptor (AhR) followed by its nuclear translocation and transcriptional activation of target genes. Another chemically diverse group of xenobiotics including phenobarbital, DDT, can activate the nuclear receptor CAR and in some cases estrogen receptors ESR1 and ESR2. We hypothesized that such chemicals can affect miRNA expression through the activation of AHR, CAR, and ESRs. To prove this statement, we used in silico methods to find DRE, PBEM, ERE potential binding sites for these receptors, respectively. We have predicted AhR, CAR, and ESRs binding sites in 224 rat, 201 mouse, and 232 human promoters of miRNA-coding genes. In addition, we have identified a number of miRNAs with predicted AhR, CAR, and ESRs binding sites that are known as oncogenes and as tumor suppressors. Our results, obtained in silico, open a new strategy for ongoing experimental studies and will contribute to further investigation of epigenetic mechanisms of carcinogenesis.

    Original languageEnglish
    Article number1750029
    Number of pages20
    JournalJournal of Bioinformatics and Computational Biology
    Issue number1
    Publication statusPublished - 1 Feb 2018


    • cancer
    • miRNA
    • xenobiotics; nuclear receptors
    • nuclear receptors
    • xenobiotics
    • MOUSE
    • CANCER
    • GENE
    • GROWTH
    • MicroRNAs/genetics
    • Computational Biology/methods
    • Estrogen Receptor beta/metabolism
    • Computer Simulation
    • Binding Sites
    • Promoter Regions, Genetic
    • Response Elements
    • Introns
    • Estrogen Receptor alpha/metabolism
    • Rats
    • Receptors, Aryl Hydrocarbon/metabolism
    • Receptors, Cytoplasmic and Nuclear/metabolism
    • Animals
    • Xenobiotics/metabolism
    • Mice
    • Software


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