Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

SiRIP140 and gene expression effects in E2-treated MCF7 cells

ABSTRACT: This experiment is designed to assess the role of RIP140 in estrogen receptor-dependent gene expression in MCF7 luminal breast cancer cells. MCF7 cells were transfected with an siRNA to target RIP140 or siControl, and subsequently depleted from hormones for three days. Thereafter, cells were treated for 6 hours with 10nM Estradiol and RNA was isolated and further processed for expression analyses.

ORGANISM(S): Homo sapiens

SUBMITTER: Gordon Brown

PROVIDER: E-MTAB-2577 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Complex formation and function of estrogen receptor α in transcription requires RIP140.

Rosell Meritxell M Nevedomskaya Ekaterina E Stelloo Suzan S Nautiyal Jaya J Poliandri Ariel A Steel Jennifer H JH Wessels Lodewyk F A LF Carroll Jason S JS Parker Malcolm G MG Zwart Wilbert W

Cancer research 20140821 19

RIP140 is a transcriptional coregulator involved in energy homeostasis, ovulation, and mammary gland development. Although conclusive evidence is lacking, reports have implicated a role for RIP140 in breast cancer. Here, we explored the mechanistic role of RIP140 in breast cancer and its involvement in estrogen receptor α (ERα) transcriptional regulation of gene expression. Using ChIP-seq analysis, we demonstrate that RIP140 shares more than 80% of its binding sites with ERα, colocalizing with i ...[more]

PMID: 25145671

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Project description:Estrogen receptor Î± (ERÎ±) is an important biomarker of breast cancer severity and a common therapeutic target. Recent studies have demonstrated that in addition to its role in promoting proliferation, ERÎ± also protects tumors against metastatic transformation. Current therapeutics antagonize ERÎ± and interfere with both beneficial and detrimental signaling pathways stimulated by ERÎ±. The goal of this study is to uncover the dynamics of coding and non-coding RNA (microRNA) expression in response to estrogen stimulation and identify potential therapeutic targets that more specifically inhibit ERÎ±-stimulated growth and survival pathways without interfering with its protective features. To achieve this, we exposed MCF7 cells (an estrogen receptor positive model cell line for breast cancer) to estrogen and prepared a time course of paired mRNA and miRNA sequencing libraries at ten time points throughout the first 24 hours of the response to estrogen. From these data, we identified three primary expression trendsâ??transient, induced, and repressedâ??that were each enriched for genes with distinct cellular functions. Integrative analysis of paired mRNA and microRNA temporal expression profiles identified miR-503 as the strongest candidate master regulator of the estrogen response, in part through suppression of ZNF217â??an oncogene that is frequently amplified in cancer. We confirmed experimentally that miR-503 directly targets ZNF217 and that over-expression of miR-503 suppresses breast cancer cell proliferation. Overall, these data indicate that miR-503 acts as a potent estrogen-induced tumor suppressor microRNA that opposes cellular proliferation and has promise as a therapeutic for breast cancer. More generally, our work provides a systems-level framework for identifying functional interactions that shape the temporal dynamics of gene expression. Quantification of miRNAs in MCF7 cells responding to estrogen following a period of estrogen starvation. Three independent biological replicates (30 samples: 3 replicates x 10 time points) of MCF7 cells were exposed to 10nM Estradiol for 0, 1, 2, 3, 4, 5, 6, 8, 12 , or 24 hours, and total RNA was extracted from the samples. Total RNA was used to generate paired RNA and miRNA sequencing. The miRNA libraries were prepared using the Bioo Scientific NextFLEX v2 library preparation kit.

Project description:Estrogen receptor Î± (ERÎ±) is an important biomarker of breast cancer severity and a common therapeutic target. Recent studies have demonstrated that in addition to its role in promoting proliferation, ERÎ± also protects tumors against metastatic transformation. Current therapeutics antagonize ERÎ± and interfere with both beneficial and detrimental signaling pathways stimulated by ERÎ±. The goal of this study is to uncover the dynamics of coding and non-coding RNA (microRNA) expression in response to estrogen stimulation and identify potential therapeutic targets that more specifically inhibit ERÎ±-stimulated growth and survival pathways without interfering with its protective features. To achieve this, we exposed MCF7 cells (an estrogen receptor positive model cell line for breast cancer) to estrogen and prepared a time course of paired mRNA and miRNA sequencing libraries at ten time points throughout the first 24 hours of the response to estrogen. From these data, we identified three primary expression trendsâ??transient, induced, and repressedâ??that were each enriched for genes with distinct cellular functions. Integrative analysis of paired mRNA and microRNA temporal expression profiles identified miR-503 as the strongest candidate master regulator of the estrogen response, in part through suppression of ZNF217â??an oncogene that is frequently amplified in cancer. We confirmed experimentally that miR-503 directly targets ZNF217 and that over-expression of miR-503 suppresses breast cancer cell proliferation. Overall, these data indicate that miR-503 acts as a potent estrogen-induced tumor suppressor microRNA that opposes cellular proliferation and has promise as a therapeutic for breast cancer. More generally, our work provides a systems-level framework for identifying functional interactions that shape the temporal dynamics of gene expression. Quantification of mRNAs in MCF7 cells responding to estrogen following a period of estrogen starvation. Three independent biological replicates (30 samples: 3 replicates x 10 time points) of MCF7 cells were exposed to 10nM Estradiol for 0, 1, 2, 3, 4, 5, 6, 8, 12 , or 24 hours, and total RNA was extracted from the samples. Total RNA was used to generate paired RNA and miRNA sequencing. RNA libraries were prepared using an Illumina TruSeq stranded mRNA library preparation kit.

Dataset Information

SiRIP140 and gene expression effects in E2-treated MCF7 cells

Publications

Complex formation and function of estrogen receptor α in transcription requires RIP140.

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