17 research outputs found

    mRNA expression levels of <i>AHR</i>, <i>AHRR</i> and <i>ARNT</i>, and of genes involved in inflammation, in MDA-MB-436 breast cancer cell line treated with two different <i>AHR</i> ligands.

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    <p>MDA-MB-436 cells were cultivated in absence (CTL) or in presence of TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin) (10<sup>-9</sup>M) or BaP (benzo[a]pyrene) (10<sup>-6</sup>M) for 16 h. Cells were then lysed and mRNA extracted. mRNA expression levels of <i>AHR</i>, <i>AHRR</i> and <i>ARNT</i> (A), and of <i>IL1B</i>, <i>IL6</i>, <i>IL8</i> and <i>CXCR4</i> (B) were determined by qRT-PCR. All experiments were performed in triplicate. Results were expressed as mean +/- s.e.m and normalized so that the mean of the control cells was 1. Three levels of statistical significance are distinguished: *p-value<0.05; **p-value<0.01; ***p-value<0.001.</p

    Immunocytochemical staining for AhR and CD4 in breast tumors.

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    <p><b>a-b</b>, moderate AhR-expressing tumor cells. Note positive AhR staining in the intratumoral stroma. <b>c-d</b>, immunostaining for AhR (c) or CD4 (d) in the same tumor sample. Immunostaining for both AhR and CD4 is observed in stromal cells in the intratumoral compartment. T, tumor cells; S, intratumoral stroma. Original Magnification, x 20.</p

    RelA knock-down by RNAi blocks TNFα-induced gene expression in HMEC cells.

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    <p>(A) Nuclear extracts from HMEC cells treated with TNF-α for the indicated periods of time were analyzed by EMSA using a <sup>32</sup>P-labeled HIV-LTR tandem κB oligonucleotide as a probe. (B) For supershift, nuclear extracts from HMEC cells treated with TNFα for 4 hours were incubated with the indicated antibodies before incubation with the labeled probe. Complex I: RelA/p50. (C) Nuclear extracts from HMEC cells stably transduced with a lentivirus encoding a shRNA targeting either RelA or a scrambled control, and treated by TNFα for the indicated periods of time were analyzed by EMSA as described in (A).</p
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