Comparative analysis of transcriptomic changes induced by zearalenone and bisphenol A in human ovarian cancer cells [microRNA_seq]
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE224107 | GEO | 2023/03/02
REPOSITORIES: GEO
Similar Datasets
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
Project description: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.
2023-03-02 | GSE224108 | GEO
Project description:Comparing the expression profiles of the genes in response to estrogen or 17b-estradiol (E2) and a mycotoxin, zearalenone (ZEA), and its analogues. Keywords: Gene expression profiling Two-condition experiment, E2- or ZEA-treated vs. control cells. 2 to 3 biological replicates, independently grown and harvested. Two to three replicates per array.
2010-09-09 | E-GEOD-15249 | biostudies-arrayexpress
Project description:Comparing the expression profiles of the genes in response to estrogen or 17b-estradiol (E2) and a mycotoxin, zearalenone (ZEA), and its analogues. Keywords: Gene expression profiling
2010-03-11 | GSE15249 | GEO
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
Project description:Exposure of humans to bisphenol A (BPA) is widespread and continuous. We previously showed that perinatal exposure to BPA increased prostate cancer risk in adult rats. Yet the effects of protracted, exposure to BPA during adulthood have not been studied. In this study, we subjected Noble rats to 32 weeks of co-treatment with testosterone (T) and BPA (low- or high-dose) or T and 17β-estradiol (E2) via Silastic capsule implants. Circulating T levels were comparable in all treatment groups, whereas the levels of free BPA were elevated in the groups that received T+low BPA (1.06 ± 0.05 ng/ml, P<0.05) and T+high BPA (10.37 ± 0.43 ng/ml, P<0.01) when compared with those in controls (0.1 ± 0.05 ng/ml). T+low/high BPA induced prostatic hyperplasia, low-grade prostatic intraepithelial neoplasia (PIN), and intraepithelial infiltration of T-lymphocytes only in the lateral prostates (LPs), whereas T+E2 induced high-grade PIN in this prostatic lobe. Genome-wide transcriptome analysis identified differential changes in the LPs of T+BPA and T+E2 treatments, with aberrant expression of multiple genes in the regulatory network controlled by the transcription factor hepatic nuclear factor 4α (HNF4α) specifically in BPA- but not E2-treated LPs. These findings suggest that the adult rat prostate is susceptible to transcriptomic reprogramming by BPA associated with the development of prostate pathology in a manner distinct from that of E2. The relevance of these data to the previous report demonstrating an association between high urinary levels of BPA and prostate cancer needs to be studied further.
2015-03-07 | GSE66633 | GEO
Project description:Zearalenone (ZEA) is a non-steroidal xenoestrogen mycotoxin produced by many Fusarium fungal species, which are common contaminants of cereal crops destined for worldwide human and animal consumption. ZEA has been linked to various male reproduction problems including decreased fertility potential. In this study, the direct impact of ZEA on the immature Sertoli TM4 cell line was evaluated. Results showed that high concentration of ZEA increase reactive oxygen species via the activation of MAPK signaling. Transcriptome analysis was performed on TM4 cell line treated with ZEA and genes involved in sex differentiation (Fgfr2, Igf1, Notch1, Sox9) and extracellular matrix (ECM) formation (Ctgf, Fam20a, Fbn1, Mmp9, Postn, Sparcl1, Spp1) were identified at the center of the functional protein association network suggesting that ZEA could be detrimental to the early steps of Sertoli cell differentiation.
2022-03-07 | GSE185111 | GEO
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
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
Project description:Bisphenol A (BPA) is primarily used to make polycarbonate plastic, with a global capacity of production exceeding 8 million tons per year. Biomonitoring studies with human urine, blood and tissue samples suggest that humans are subjected to widespread and continuous exposure to BPA. It has been well established that early life exposure to BPA predisposes the prostate gland to carcinogenesis later in life. However, it remains unknown if BPA exposure during adulthood induces benign or neoplastic pathology in the prostate. The main objective of the present study is to determine the effects of BPA exposures during adulthood on the prostate and to characterize the global transcriptional reprogramming underlying endocrine disruption by BPA. We elevated circulating levels of free BPA in Noble rats to the human-relevant internal dose range with BPA-filled Silastic implants while maintaining the physiological levels of testosterone (T) with T-filled implants. Cotreatment with T and 17β-estradiol (E2) was our reference regimen which induced preneoplastic and cancereous lesions. The T + low/high dose of BPA induced prostatic hyperplasia, low-grade prostate intraepithelial neoplasia (LGPIN) and intraepithelial infiltration of T-lymphocytes specifically in the lateral prostate (LP). Using microarray analysis, we delineated specific impacts of low and high dose of BPA (with the T-support) on the gene expression program in LPs. Hierarchical clustering revealed that the endocrine disrupting effects of T + low dose of BPA showed partial resemblance to those of T + high dose of BPA and T+E2. In contrast, the influence of T+ high dose of BPA on the LP transcriptome was completely different from those of T + E2. Further, IPA analysis of specific T+ low or high BPA gene signature identified a transcription factor, HNF4α, as a regulatory hub affecting a number of differentially expressed genes by BPA exposures. These findings suggest that the adult rat prostate is still venerable to the endocrine disrupting effects of BPA. Perhaps chronic exposure to low dose of BPA provides a niche comprising heightened cell proliferation, inflammatory responses and disrupted gene expression program, which favor the onset and development of prostatic benign or malignant diseases in men. Rat lateral prostates were collected from untreated control and treated groups [Testosterone (T) + Estradiol (E2), T + low dose Bisphenol A (low BPA) and T + high BPA] for RNA extraction and hybridization on Affymetrix microarrays. We sought to identify transcriptional signature of BPA exposures in the lateral prostate gland.
2015-03-07 | E-GEOD-66633 | biostudies-arrayexpress