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Xenoestrogen-induced epigenetic repression of non-coding microRNA genes in breast epithelial cells

ABSTRACT: Early exposure to xenoestrogens may predispose to breat cancer risk later in adult life. The long-lived, self-regenerating epithelial progenitor cells are more susceptible to these exposure injuries and transmit the injured memory throught epigenetic mechanisms to their differentiated progeny. We have established a breast progenitor model for epigenetic study and our previous work demonstrated that DNA methylation profiling of epithelial progeny derived from progenitors exposed to estradiol detected hypermethylated loci in 0.5% of protein-coding genes. In this study, we extended this exposure study to non-coding microRNA genes.

ORGANISM(S): Homo sapiens

PROVIDER: GSE16001 | GEO | 2012/04/16

SECONDARY ACCESSION(S): PRJNA115417

REPOSITORIES: GEO

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Xenoestrogen-induced epigenetic repression of non-coding microRNA genes in breast epithelial cells

Project description:Early exposure to xenoestrogens may predispose to breat cancer risk later in adult life. The long-lived, self-regenerating epithelial progenitor cells are more susceptible to these exposure injuries and transmit the injured memory throught epigenetic mechanisms to their differentiated progeny. We have established a breast progenitor model for epigenetic study and our previous work demonstrated that DNA methylation profiling of epithelial progeny derived from progenitors exposed to estradiol detected hypermethylated loci in 0.5% of protein-coding genes. In this study, we extended this exposure study to non-coding microRNA genes. Three mammosphere-derived epithelial cell (MDEC) sample sets from three independent patients. Each sample set includes one DES-preexposed and one DMSO-preexposed MDEC.

2012-04-15 | E-GEOD-16001 | biostudies-arrayexpress

Differential DNA methylation profiles in estrogen-pre-exposed breast epithelial cells

2007-12-01 | GSE7844 | GEO

Differential DNA methylation profiles in estrogen-pre-exposed breast epithelial cells

Project description:This study tried to determine whether exposure of breast stem/progenitor cells to estrogen disrupts the epigenome of progeny epithelial cells. DNA methylation profiles were compared between control and pre-exposed epithelial cells using a genome-wide detection method called MeDIP-chip. Keywords: MeDIP-chip Breast stem/progenitor cells were continuously exposed to 17beta-estradiol (E2, 70 nM) or DMSO (vehicle control) for two weeks and then placed on 2-dimensional collagen substratum for 2-3 weeks for epithelial cell differentiation. DNA from control and pre-exposed cells were extracted and MeDIP ssays were performed using antibodies against 5-methylcytosine. The immunoprecipitated and input DNA were used to probe the Agilent human CpG island microarray. Dye-swap experiments were also performed.

2007-11-30 | E-GEOD-7844 | biostudies-arrayexpress

Elucidation of xenoestrogen metabolism by non-targeted, stable isotope-assisted mass spectrometry in breast cancer cells

Project description:Environmental exposure to xenoestrogens, i.e., chemicals that imitate the hormone 17β-estradiol, has the potential to influence hormone homeostasis and action. Detailed knowledge of xenobiotic biotransformation processes in cell models is key when transferring knowledge learned from in vitro models to in vivo relevance. This study elucidated the metabolism of two naturally-occurring phyto- and myco-estrogens; namely genistein and zearalenone, in an estrogen receptor positive breast cancer cell line (MCF-7) with the aid of stable isotope-assisted metabolomics and the bioinformatic tool MetExtract II. Metabolism was studied in a time course experiment after 2, 6 and 24 h incubation. Twelve and six biotransformation products of zearalenone and genistein were detected, respectively, clearly demonstrating the abundant xenobiotic biotransformation capability of the cells. Zearalenone underwent extensive phase-I metabolism resulting in α-zearalenol (α-ZEL), a molecule known to possess a significantly higher estrogenicity, and several phase-II metabolites (sulfo- and glyco-conjugates) of the native compound and the major phase I metabolite α-ZEL. Moreover, potential adducts of zearalenone with a vitamin and several hydroxylated metabolites were annotated. Genistein metabolism resulted in sulfation, combined sulfation and hydroxylation, acetylation, glucuronidation and unexpectedly adduct formation with pentose- and hexose-sugars. Kinetics of metabolite formation and subsequent excretion into the extracellular medium revealed a time-dependent increase in most biotransformation products. The untargeted elucidation of biotransformation products formed during cell culture experiments enables an improved and more meaningful interpretation of toxicological assays and has the potential to identify unexpected or unknown metabolites.

2023-10-26 | MTBLS2716 | MetaboLights

Identifying dormant Nfatc1-marked stem/progenitor cells as an important contributor for mammary lobuloalveoli formation

Project description:The Mammary gland undergoes complicated epithelial remodeling to form lobuloalveoli during pregnancy, in which basal epithelial cells remarkably increase to form a basket-like architecture. However, it remains largely unknown how dormant mammary basal stem/progenitor cells involve in lobuloalveolar development. Here, we show that Nfatc1 expression marks a rare population of mammary epithelial cells with the majority being basal epithelial cells. Nfatc1 reporter-marked basal epithelial cells are relatively dormant mammary stem/progenitor cells. Although Nfatc1 reporter-marked basal epithelial cells show limited contribution to the homeostasis of mammary epithelium, they divide rapidly during pregnancy and contribute to lobuloalveolar development. Furthermore, Nfatc1 reporter-marked basal epithelial cells are preferentially used for multiple pregnancies. Using single-cell RNA-seq analysis, we identify multiple functionally distinct clusters within the Nfatc1 reporter-marked cell-derived progeny cells during pregnancy. Taken together, our findings underscore Nfatc1 reporter-marked basal cells as dormant stem/progenitor cells that contribute to mammary lobuloalveolar development during pregnancy.

2022-02-18 | GSE175432 | GEO

Genome wide map of SOX1 occupancy in human embryonic stem cell derived neural progenitors

Project description:To understand how SOX1's binding profile in neural progenitor with different regional identities, we differentiated hESC into neural progenitors with rostral and caudal identies throught modulating Wnt signaling pathway. We collected cells at neural differentiation day 4 and 8, and performed SOX1 ChIP-seq to investigate SOX1's genome wide binding profiles. These results provide important information for the mechanism underlying SOX1's functions in early regionalization.

2020-08-26 | GSE138215 | GEO

Human breast tumor

Project description:subpopulation of breat cancer using gene expression data and clinical data Keywords: breast cancer survival and metastasis analysis

2006-06-28 | GSE2845 | GEO

Sparus aurata gut microbiota

Project description:Vaccinated gilthead seabream after continuous oral exposure to xenoestrogens Raw sequence reads

| PRJNA749661 | ENA

Preferential Epigenetic Programming of Estrogen Response after in utero xenoestrogen (bisphenol-A) exposure [NimbleGen]

Project description:Bisphenol-A (BPA) is an environmentally ubiquitous estrogen-like endocrine-disrupting compound. Exposure toBPAin utero hasbeen linked tofemale reproductive disorders, including endometrial hyperplasiaandbreast cancer. Estrogens are an etiological factor in many of these conditions. We sought to determine whether in utero exposure to BPA altered the globalCpGmethylation pattern of the uterine genome, subsequent gene expression, and estrogen response.Pregnantmicewere exposed to an environmentally relevant dose of BPAorDMSOcontrol.Uterine DNAand RNAwere examined by usingmethylatedDNAimmunoprecipitationmethylation microarray, expression microarray, and quantitative PCR. In utero BPA exposure altered the global CpG methylation profile of the uterine genome and subsequent gene expression. The effect on gene expression was not apparent until sexual maturation, which suggested that estrogen response was the primary alteration. Indeed, prenatal BPA exposure preferentially altered adult estrogen-responsive gene expression. Changes in estrogen response were accompanied by altered methylation that preferentially affected estrogen receptor-a (ERa)–binding genes. The majority of genes that demonstrated both altered expression and ERa binding had decreased methylation. BPA selectively altered the normal developmental programming of estrogen-responsive genes via modification of the genes that bind ERa. Gene– environment interactions driven by early life xenoestrogen exposure likely contributes to increased risk of estrogenrelateddisease in adults.—Jorgensen, E. M.,Alderman,M.H., III,Taylor, H. S. Preferential epigenetic programmingof estrogen response after in utero xenoestrogen (bisphenol-A) exposure.

2016-10-24 | GSE89125 | GEO

Preferential Epigenetic Programming of Estrogen Response after in utero xenoestrogen (bisphenol-A) exposure [Illumina]

Project description:Bisphenol-A (BPA) is an environmentally ubiquitous estrogen-like endocrine-disrupting compound. Exposure toBPAin utero hasbeen linked to female reproductive disorders, including endometrial hyperplasia and breast cancer. Estrogens are an etiological factor in many of these conditions. We sought to determine whether in utero exposure to BPA altered the global CpG methylation pattern of the uterine genome, subsequent gene expression, and estrogen response. Pregnant mice were exposed to an environmentally relevant dose of BPA or DMSO control. Uterine DNA and RNA were examined by using methylated DNA immunoprecipitation methylation microarray, expression microarray, and quantitative PCR. In utero BPA exposure altered the global CpG methylation profile of the uterine genome and subsequent gene expression. The effect on gene expression was not apparent until sexual maturation, which suggested that estrogen response was the primary alteration. Indeed, prenatal BPA exposure preferentially altered adult estrogen-responsive gene expression. Changes in estrogen response were accompanied by altered methylation that preferentially affected estrogen receptor-a (ERa)–binding genes. The majority of genes that demonstrated both altered expression and ERa binding had decreased methylation. BPA selectively altered the normal developmental programming of estrogen-responsive genes via modification of the genes that bind ERa. Gene– environment interactions driven by early life xenoestrogen exposure likely contributes to increased risk of estrogen related disease in adults.—Jorgensen, E. M.,Alderman,M.H., III,Taylor, H. S. Preferential epigenetic programmingof estrogen response after in utero xenoestrogen (bisphenol-A) exposure.

2016-09-15 | GSE86923 | GEO

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