Analysis of estrogen-induced mRNA in endometrial cancer cells with forced expression of ER
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE197905 | GEO | 2022/03/08
REPOSITORIES: GEO
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Project description:Unopposed estrogen stimulation and insulin resistance are known to play important roles in endometrial cancer (EC), but the relationship between these two factors and how they contribute to endometrial lesions is not completely understood. To investigate the endometrial transcriptome profiles and the associated molecular pathway alterations, we established an ovariectomized C57BL/6 mouse model treated with subcutaneous implantation of the 17-β estradiol (E2) pellet and/or high-fat diet (HFD) to mimic sustained estrogen stimulation and insulin resistance. We used microarrays to detail the global program of gene expression underlying the mice endometrium and indentified distinct classes of E2 and/or high-fat diet related ncRNA during this process.
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Project description:Endometrial estrogen receptor-α (ESR1) is indispensable for epithelial and stromal proliferation and differentiation during decidualization, yet the gene targets of estradiol (E2) / ESR1 in human stromal cells and associated mechanisms remain unknown. In this study, we characterized global E2-ESR1‒dependent transcriptomic changes and ESR1 recruitment to chromatin. Human endometrial stromal cells were isolated from 4 premenopausal women for primary cell culture. Genome-wide RNA expression by RNA-sequencing was compared in endometrial stromal cells with or without siRNA knockdown of ESR1 in the presence or absence of E2 (n=2). Genome-wide recruitment of ESR1 to chromatin was assessed by chromatin immunoprecipitation sequencing using an antibody against ESR1 was performed to examine binding to target genes (n=1).
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Project description:To investigate the role of ARID1A in estrogen receptor positive endometrial cancers, we performed RNAseq in control and ARID1A-knockdown Ishikawa cells treated with DMSO,E2 and E2+Fulvestrant for 8 hours.
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Project description:Combination therapy with estrogen and a selective estrogen receptor modulator (SERM) is a promising approach to safely alleviate important side effects related to estrogen deficiency in women at high risk for breast cancer. Data related to endometrial safety of estrogen+SERM co-therapies are limited, however. The primary goal of this study was to evaluate the endometrial profile of low-dose E2 and Tam alone and in combination. In this study 16 postmenopausal female cynomolgus macaques were randomized to receive placebo, low-dose micronized estradiol (E2, 0.25 mg/1800 kcal), the SERM tamoxifen (Tam, 20 mg/1800 kcal), or E2+Tam in a parallel-arm design. Endometrial samples were collected after 4 months of treatment and used for microarray analysis.
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Project description:SET is a multifunctional histone-binding oncoprotein that regulates transcription by an unclear mechanism. Here, we show that SET enhances estrogen-dependent transcription. SET knockdown abrogates transcription of estrogen-responsive genes and their enhancer RNAs (eRNAs). In response to 17β-estradiol (E2), SET binds to the estrogen receptor α (ERα) and is recruited to estrogen receptor α (ERα)-bound enhancers and promoters at estrogen response elements (EREs). SET functions as a histone H2 chaperone that dynamically associates with H2A.Z via its acidic C-terminal domain and promotes H2A.Z incorporation, ERα, MLL1 and KDM3A loading and modulates histone methylation at EREs. SET depletion diminishes recruitment of condensin complexes to EREs and impairs E2-dependent enhancer-promoter looping. Thus, SET boosts E2-induced gene expression by establishing an active chromatin structure at ERα-bound enhancers and promoters, which is essential for transcriptional activation.
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Project description:SET is a multifunctional histone-binding oncoprotein that regulates transcription by an unclear mechanism. Here, we show that SET enhances estrogen-dependent transcription. SET knockdown abrogates transcription of estrogen-responsive genes and their enhancer RNAs (eRNAs). In response to 17β-estradiol (E2), SET binds to the estrogen receptor α (ERα) and is recruited to estrogen receptor α (ERα)-bound enhancers and promoters at estrogen response elements (EREs). SET functions as a histone H2 chaperone that dynamically associates with H2A.Z via its acidic C-terminal domain and promotes H2A.Z incorporation, ERα, MLL1 and KDM3A loading and modulates histone methylation at EREs. SET depletion diminishes recruitment of condensin complexes to EREs and impairs E2-dependent enhancer-promoter looping. Thus, SET boosts E2-induced gene expression by establishing an active chromatin structure at ERα-bound enhancers and promoters, which is essential for transcriptional activation.
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Project description:Tamoxifen, a small molecule inhibitor that binds the Estrogen Receptor alpha (ERα), blocks breast cancer progression while increasing the risk for endometrial cancer. In this study, we assessed genome-wide ERα-chromatin interactions in surgical specimens of endometrial tumors from patients who were previously treated for breast cancer with tamoxifen, and endometrial tumors from patients who were treated without tamoxifen. We compared ERα and signal at differential ERα sites in endometrial tumors of nine patients who received tamoxifen with endometrial tumors with six patients who never used tamoxifen. In addition, we performed H3K27ac (a marker for activity) ChIPs on the above mentioned endometrial tumors, and assed this signal at differential ERα sites. Compared to endometrial tumors of non-users, tamoxifen-associated endometrial tumors exposed higher H3K27ac intensities at ERα sites that are enriched in tamoxifen-associated endometrial tumors. Four tamoxifen-associated endometrial tumors that we used in our analysis have been previously published as Tumor A, B, D, and E in GSE81213.
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Project description:Tamoxifen, a small molecule inhibitor that binds the Estrogen Receptor alpha (ERα), blocks breast cancer progression while increasing the risk for endometrial cancer. In this study, we assessed genome-wide ERα-chromatin interactions in surgical specimens of endometrial tumors from patients who were previously treated for breast cancer with tamoxifen, and endometrial tumors from patients who were treated without tamoxifen. We compared ERα and signal at differential ERα sites in endometrial tumors of nine patients who received tamoxifen with endometrial tumors with six patients who never used tamoxifen. In addition, we performed H3K27ac (a marker for activity) ChIPs on the above mentioned endometrial tumors, and assed this signal at differential ERα sites. Compared to endometrial tumors of non-users, tamoxifen-associated endometrial tumors exposed higher H3K27ac intensities at ERα sites that are enriched in tamoxifen-associated endometrial tumors. Four tamoxifen-associated endometrial tumors that we used in our analysis have been previously published as Tumor A, B, D, and E in GSE81213.
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Project description:Breast cancer is one of the most prevalent cancers in women worldwide. Through the regulation of many coding and non-coding target genes, estrogen (E2 or 17b-estradiol) and its nuclear receptor ERα play important roles in breast cancer development and progression. Despite intensive studies on estrogen-regulated coding genes over the past decades, molecular mechanisms underlying estrogen-regulated non-coding RNAs in breast cancer remain to be elucidated. Here, we performed extensive epigenomic studies including GRO-seq and ATAC-seq, and identified genome-wide estrogen-regulated long non-coding RNAs (lncRNAs). Similar to the coding targets of ERα, the transcription of estrogen-regulated lncRNAs correlates with the activation status of ERα-bound enhancers, measured by eRNA production, chromatin accessibility, and the occupancy of the enhancer regulatory components including P300, MED1, and ARID1B. Our 3D chromatin architecture analyses suggest that lncRNAs and their neighboring E2-resonsive coding genes, exemplified by LINC00160 and RUNX1, might be regulated as a 3D structural unit resulted from enhancer-promoter interactions. Finally, we evaluated the expression levels of LINC00160 and RUNX1 in various types of breast cancer and found that their expression positively correlated with the survival rate in ER+ breast cancer patients, implying that the estrogen-regulated LINC00160 and its neighboring RUNX1 might represent potential biomarkers for ER+ breast cancers.
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