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Comparative analysis of transcriptomic changes induced by zearalenone and bisphenol A in human ovarian cancer cells

ABSTRACT: Xenoestrogens are natural or synthetic compounds that mimic the effect of endogenous estrogens and might cause cancer. We aimed to compare the global transcriptomic response to zearalenone (ZEA; mycotoxin) and bisphenol A (BPA; plastic additive) with the effect of physiological estradiol (E2) in the PEO1 human ovarian cell line by mRNA and microRNA sequencing. Estrogen exposure induced remarkable transcriptomic changes: 308, 288 and 63 genes were upregulated (log2FC > 1); 292, 260 and 45 genes were downregulated (log2FC < -1) in response to E2 (10 nM), ZEA (10 nM) and BPA (100 nM), respectively. Furthermore, the expression of 13, 11 and 10 miRNAs changed significantly (log2FC > 1, or log2FC < -1) after exposure to E2, ZEA and BPA, respectively. Functional enrichment analysis of the significantly differentially expressed genes and miRNAs revealed several pathways related to the regulation of cell proliferation and migration. The effect of E2 and ZEA was highly comparable: 407 genes were coregulated by these molecules. We could identify 83 genes that were regulated by all three treatments that might have a significant role in the estrogen response of ovarian cells. Furthermore, the downregulation of several miRNAs (miR-501-5p, let-7a-2-3p, miR-26a-2-3p, miR-197-5p and miR-582-3p) was confirmed by qPCR, which might support the proliferative effect of estrogens in ovarian cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE224108 | GEO | 2023/03/02

REPOSITORIES: GEO

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Comparative analysis of transcriptomic changes induced by zearalenone and bisphenol A in human ovarian cancer cells [microRNA_seq]

Project description:In this study we compared the effect of zeralenone (ZEA; mycotoxin) and bisphenol A (BPA; plastic additive) to the global microRNA expression of human ovarian cells with the effect of physiological estradiol (E2). For this purpose we applied the PEO1 human ovarian cell line that was treated with 10 nM ZEA, 100 nM BPA and 10 nM E2. MicroRNA expression was compared by microRNA sequencing (Illumina NextSeq 500).

2023-03-02 | GSE224107 | GEO

Comparative analysis of transcriptomic changes induced by zearalenone and bisphenol A in human ovarian cancer cells [mRNA_seq]

Project description:In this study we compared the global transcriptomic response of human ovarian cells to zeralenone (ZEA; mycotoxin) and bisphenol A (BPA; plastic additive) with the effect of physiological estradiol (E2). For this purpose we applied the PEO1 human ovarian cell line that was treated with 10 nM ZEA, 100 nM BPA and 10 nM E2. Transcriptomic profile was compared by mRNA sequencing (Illumina NextSeq 500).

2023-03-02 | GSE224105 | GEO

Mouse placental microRNA profiling upon zearalenone exposure

Project description:Mycoestrogens are derived from mold and can interfere with female reproduction. Mycoestrogen zearalenone (ZEA) is a common food contaminant in levels of ppb ~ low ppm. Previously we demonstrated disrupted mouse placental development by 40 ppm ZEA diet. MicroRNAs are sensitive to xenobiotics and have been implicated in placental physiology and pathology. We hypothesized that ZEA could dysregulate microRNA expression in the mouse placenta. Gestation day 13.5 (D13.5) placentas from young mice treated with 0 ppm (control), 4 ppm, and 40 ppm ZEA diets were analyzed for microRNA profiling using microRNA array. The top 20 most highly expressed microRNAs in the D13.5 control placentas are predicated to target genes involved in important signaling pathways that are critical for maternal-fetal communications, such as protein processing in endoplasmic reticulum, endocytosis, and regulation of actin cytoskeleton. Using criteria of Log2FC ≥ 1 and Log2FC ≤ -1 (linear 2 fold change (FC)), a false discovery rate adjusted p-value ≤ 0.05, and average reading > 100 (top 20% most abundant microRNAs), R package limma identified 8 differentially expressed miRNAs (mmu-miR-133b-5p, mmu-miR-7028-5p, mmu-miR-294-3p, mmu-miR-3970, mmu-miR-20b-5p, mmu-miR-7683-3p, mmu-miR-291b-3p, mmu-miR-369-3p) in the 40 ppm ZEA group that included all 4 differentially expressed miRNAs in the 4 ppm ZEA group. Some of these differentially expressed microRNAs have been shown in vitro to have important functions in placental growth and maternal-fetal transport. These data imply roles of placental microRNAs in regulating expression of genes critical for placental function in vivo and in sensing environmental contaminants.

2019-09-11 | GSE137242 | GEO

Genistein and bisphenol A exposure cause estrogen receptor 1 to bind thousands of binding sites in a cell type-specific manner

Project description:To obtain an integrated view of gene regulation in response to environmental and endogenous estrogens on a genome-wide scale, we performed ChIP-seq, to identify estrogen receptor 1 (ER) binding sites, and RNA-seq in endometrial cancer cells exposed to bisphenol A (BPA; found in plastics), genistein (GEN; found in soybean), or 17β-estradiol (E2; an endogenous estrogen). GEN and BPA treatment induces thousands of ER binding sites and >50 gene expression changes, representing a subset of E2‑induced gene regulation changes. Genes affected by E2 were highly enriched for ribosome-associated proteins; however, GEN and BPA failed to regulate most ribosome-associated proteins and instead enriched for transporters of carboxylic acids. Treatment-dependent changes in gene expression were associated with treatment-dependent ER binding sites, with the exception that many genes up-regulated by E2 harbored a BPA-induced ER binding site, but failed to show any expression change after BPA treatment. GEN and BPA exhibited a similar relationship to E2 in the breast cancer line T-47D, where cell type specificity played a much larger role than treatment specificity. Overall, both environmental estrogens clearly regulate gene expression through ER on a genome-wide scale, although with lower potency resulting in less ER binding sites and less gene expression changes compared to the endogenous estrogen, E2.

2012-06-13 | GSE38234 | GEO

Genistein and bisphenol A exposure cause estrogen receptor 1 to bind thousands of binding sites in a cell type-specific manner

2012-06-13 | E-GEOD-38234 | biostudies-arrayexpress

Uterine gene profiles from WT, KIKO (DNA-binding deficient ERα) and aERKO mice treated with estradiol or xenoestrogens

Project description:Ovariectomized WT, KIKO (DNA-binding deficient ERα) or αERKO female mice were injected (ip) with saline (vehicle), estradiol (E2; 250 ng), bisphenol A (BPA; 750 µg) or 2,2-bis(p-hydroxyphenyl)-1,1,1-trichloroethane (HPTE; 750 µg) and uteri were collected after 2 or 24 hours. Uterine profiles were compared and indicated the early (2 hour) responses to E2 were highly correlated to the BPA and HPTE profiles. KIKO patterns included overlap with WT but also included distinct responses. Later (24 hour) responses in the KIKO were weaker, indicating DNA binding is needed to maintain the estrogenic response. BPA and HPTE also showed a weakened late response in the WT, suggesting they are impeded estrogens.

2009-12-01 | GSE18168 | GEO

miR-625-3p regulates oxaliplatin resistance by targeting MAP2K6-p38 signaling in human colorectal adenocarcinoma cells

Project description:Oxaliplatin (oxPt) resistance in colorectal cancers (CRC) is a major unsolved problem. Consequently, predictive markers and a better understanding of resistance mechanisms are urgently needed. To investigate if the recently identified predictive miR-625-3p is functionally involved in oxPt resistance, stable and inducible models of miR-625-3p dysregulation were analyzed. Ectopic expression of miR-625-3p in CRC cells led to increased resistance towards oxPt. The mitogen-activated protein kinase (MAPK) kinase 6 (MAP2K6/MKK6) – an activator of p38 MAPK - was identified as a functional target of miR-625-3p, and, in agreement, was down-regulated in patients not responding to oxPt therapy. The miR-625-3p resistance phenotype could be reversed by anti-miR-625-3p treatment and by ectopic expression of a miR-625-3p insensitive MAP2K6 variant. Transcriptome, proteome and phosphoproteome profiles revealed inactivation of MAP2K6-p38 signaling as a possible driving force behind oxPt resistance. We conclude that miR-625-3p induces oxPt resistance by abrogating MAP2K6-p38 regulated apoptosis and cell cycle control networks.

2017-03-29 | MSV000080762 | MassIVE

Expression analysis of ovarian cancer cell line

Project description:The aim of this analysis is searching the target gene of miR-135a-3p in ovarian cancer cell line. The gene expression of cell line with overexpressed miR-blank or miR-135a-3p was compared. Three ovarian cancer cell lines were enrolled this study. Those cells were transfected with miR-blank as control or miR-135a-3p.

2016-07-23 | E-GEOD-84723 | biostudies-arrayexpress

The effect of bisphenol A on human prostaspheres derived from primary prostate epithelial cells

Project description:Bisphenol A is an environmental xenoestrogen commonly known as an endocrine disruptor. We previously reported BPA-treated human primary prostate epithelial cell derived prostaspheres had larger size, exhibited clonogenicity, and showed increase in stem cell marker expression. Results reveal the molecular basis of BPA action in human prostate stem-progenitor cells. Human primary prostate epithelial cells from three disease-free Caucasian donors formed prostaspheres from single stem-like cells in matrigel cultures and were treated with 0.1 nM estradiol-17β (E2), 10 nM (B10), 200 nM (B200), and 1000 nM bisphenol A (BPA) for 7 days. The vehicle-treated prostaspheres were used as 'untreated controls'.

2014-11-05 | E-GEOD-62953 | biostudies-arrayexpress

Transcriptomal effects of four-day exposure to estradiol on mouse primary culture urogenital sinus mesenchymal cells of fetal mouse prostate

Project description:Developmental exposure of mouse fetuses to estrogens results in dose-dependent permanent effects on prostate morphology and function. Fetal prostatic mesenchyme cells express estrogen receptor alpha (ERα) and androgen receptors and convert stimuli from estrogens and androgens into signaling to regulate epithelial cell proliferation and differentiation. To obtain mechanistic insight into the role of different doses of estradiol (E2) in regulating mesenchymal cells, we examined E2-induced transcriptomal changes in primary cultures of fetal mouse prostate mesenchymal cells. Urogenital sinus mesenchyme cells were obtained from male mouse fetuses at gestation day 17 and exposed to 10 pM, 100 pM or 100 nM E2 in the presence of a physiological concentration of dihydrotestosterone (0.69 nM) for four days. Gene ontology studies suggested that low doses of E2 (10 pM and 100 pM) induce genes involved in cell adhesion, morphological tissue development, and sterol biosynthesis but suppress genes involved in growth factor signaling and cell adhesion. Genes showing inverted-U-shape dose responses (enhanced by E2 at 10 pM E2 but suppressed at 100 pM) were identified, and their enrichment in the glycolytic pathway was demonstrated. At the highest dose (100 nM), E2 induced genes enriched not only for cell adhesion but also steroid hormone signaling and metabolism, cytokines and their receptors, cell-to-cell communication, Wnt signaling, and TGF-β signaling. These results suggest that prostate mesenchymal cells may regulate epithelial cells through direct cell contacts when estrogen level is low whereas soluble growth factors might play significant roles when estrogen level is high.

2012-03-21 | GSE36630 | GEO

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