<i>CYP1A1</i>, <i>CYP1A2</i>, <i>CYP1B</i>1 and <i>AhR</i> mRNA expression in PHHs (n = 5) incubated with 1, 10, 100 μM skatole or 10 nM TCDD for 8 or 24 hours.

<p><i>CYP1A1</i>, <i>CYP1A2</i>, <i>CYP1B</i>1 and <i>AhR</i> mRNA expression in PHHs (n = 5) incubated with 1, 10, 100 μM skatole or 10 nM TCDD for 8 or 24 hours.</p

Skatole increases CYP1A1 expression in HepG2-C3 cells and PHHs.

<p>RT-qPCR analysis of <i>CYP1A1</i> (A) and <i>AhR</i> (B) mRNA expression following incubation of HepG2-C3 cells with 1, 10 or 100 μM skatole for 2, 4, 8 or 24 h (n = 3). (C) CYP1A and actin protein expression in PHHs (Donor #400) after incubation with 10, 50 or 100 μM for 24 h. * Significantly different from time-matched control cells (no treatment) (Student’s t–test; p < 0.001).</p

Primer sequences.

<p>Primer sequences.</p

Indole-3-carbinol (I3C) induces CYP1A1 expression and activates AhR.

<p>(A) RT-qPCR analysis of <i>CYP1A1</i> mRNA expression in HepG2-C3 cells incubated with 0.1, 1 or 10 μM I3C for 24 h (n = 3). (B) Relative luciferase activity measured in HAhLH or HepAhLH cells incubated with I3C (from 1.10−⁷ M to 1.10−⁴ M) for 8 h (n = 3). (C) RT-qPCR analysis of <i>CYP1A1</i> mRNA expression in HepG2-C3 cells incubated with 10 nM TCDD alone or in the presence of 0.1, 1 or 10 μM I3C (n = 3). Bars not sharing subscription are significantly different (p < 0.05).</p

Straightforward sustainable synthesis of novel non-endocrine disruptive bio-based organic UV-B filters with antimicrobial activity

With an increasing demand for safe and natural products from both industries and consumers, paired with the recent ban of decried molecules (i.e. octinoxate, avobenzone or octocrylene) due to their high negative impact on humans and the environment (i.e. endocrine disruption, coral bleaching), safe bio-based alternatives are a necessary and promising surrogate to substitute current commercialized petroleum-based UV filters. In this context, a class of bio-based molecules, displaying interesting UV-B filtering properties and great photostability were developed from furfural and 5-hydroxymethylfurfural (HMF), using the Knoevenagel condensation with a set of green conditions to minimize the impact on environment. Furthermore, those furfural- and HMF-based molecules demonstrated antimicrobial properties as secondary activity, highly sought by industries. Some furan derivatives being recognized to exhibit toxicological risks, in silico and in vitro assays were conducted and demonstrated the absence of endocrine disruption activity for these new molecules.</p

Immunocytochemical analysis of the effects of prenyltransferase inhibitors on estrogen receptor (ER) α distribution in MCF-7 cells

<p><b>Copyright information:</b></p><p>Taken from "Prenylation inhibitors stimulate both estrogen receptor α transcriptional activity through AF-1 and AF-2 and estrogen receptor β transcriptional activity"</p><p>Breast Cancer Research 2004;7(1):R60-R70.</p><p>Published online 8 Nov 2004</p><p>PMCID:PMC1064103.</p><p>Copyright © 2004 Cestac et al., licensee BioMed Central Ltd.</p> Cells, deprived of estradiol (E2) for 7 days, were treated or not with FTI-277 (10 μM or dithiothreitol/dimethylsulfoxide vehicle), and 24 hours later they were stimulated with E2 (5 nM) or ethanol and treated or not with FTI-277 or GGTI-298 (10 μM or 5 μM, respectively, or vehicle). After 24 hours, cells were fixed and stained. One randomly selected field is presented for each treatment. Data were quantified by determining the grey value of both the nucleus and the cytoplasm for each cell counted, as described in Materials and methods. For each experimental condition, six randomly selected fields were analyzed. The total number of cells present in the fields ranged from 250 to 400. Error bars indicate the mean values ± standard error of the mean, and the results are representative of two independent experiments

Effects of prenyltransferase inhibitors on estrogen response element-dependent luciferase activity in HELN cells, transfected with estrogen receptor (ER) α or its mutants

<p><b>Copyright information:</b></p><p>Taken from "Prenylation inhibitors stimulate both estrogen receptor α transcriptional activity through AF-1 and AF-2 and estrogen receptor β transcriptional activity"</p><p>Breast Cancer Research 2004;7(1):R60-R70.</p><p>Published online 8 Nov 2004</p><p>PMCID:PMC1064103.</p><p>Copyright © 2004 Cestac et al., licensee BioMed Central Ltd.</p> Cells, deprived of estradiol (E2) for 4 days, were co-transfected with the Renilla luciferase plasmid and either HEG0 (full-length ERα), HEG19 (AF-1-deleted ERα), HEG7 (AF-2-deleted ERα) or pSG5 (empty vector). Five hours after transfection, cells were treated or not with FTI-277 (10 μM or dithiothreitol/dimethylsulfoxide vehicle), and 24 hours later they were stimulated with E2 (5 nM) or ethanol and treated or not with FTI-277 or GGTI-298 (10 μM or 5 μM, respectively, or dithiothreitol/dimethylsulfoxide vehicle). Luciferase activity was quantified 16 hours after E2 addition, as described in Materials and methods. Results are expressed in arbitrary units after normalization. Error bars indicate the mean values ± standard deviation from triplicate experiments, and the results are representative of three independent experiments. Results obtained show that prenylation inhibitors statistically increase or do not statistically increase the luciferase activity on their own compared with control cells (white bars) and statistically increase the luciferase activity induced by E2 compared with the activity induced by E2 alone (grey bars) in HELN cells transfected with ERα or its mutants (* < 0.02)

DTBP-Endocrinology-Supplemental Materials.pdf

Supplemental materials supporting the manuscript entitled, "2,4-Di-tert-butylphenol Induces Adipogenesis in Human Mesenchymal Stem Cells by Activating Retinoid X Receptors" This file includes Figure S1, Figure S2, Figure S3 and Table S1</p

Potential Role of Estrogen Receptor Beta as a Tumor Suppressor of Epithelial Ovarian Cancer

<div><p>Ovarian cancer is the gynecological cancer exhibiting the highest morbidity and improvement of treatments is still required. Previous studies have shown that Estrogen-receptor beta (ERβ) levels decreased along with ovarian carcinogenesis. Here, we present evidence that reintroduction of ERβ in BG-1 epithelial ovarian cancer cells, which express ERα, leads <em>in vitro</em> to a decrease of basal and estradiol-promoted cell proliferation. ERβ reduced the frequency of cells in S phase and increased the one of cells in G2/M phase. At the molecular level, we found that ERβ downregulated total retinoblastoma (Rb), phosphorylated Rb and phospho-AKT cellular content as well as cyclins D1 and A2. In addition, ERβ had a direct effect on ERα, by strongly inhibiting its expression and activity, which could explain part of the anti-proliferative action of ERβ. By developing a novel preclinical model of ovarian cancer based on a luminescent orthotopic xenograft in athymic Nude mice, we further revealed that ERβ expression reduces tumor growth and the presence of tumor cells in sites of metastasis, hence resulting in improved survival of mice. Altogether, these findings unveil a potential tumor-suppressor role of ERβ in ovarian carcinogenesis, which could be of potential clinical relevance for the selection of the most appropriate treatment for patients.</p> </div