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ABSTRACT: 3' mRNA sequencing of MCF7 cells upon E2 induction

PROVIDER: PRJNA1196847 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31677539.fastq.gz	Fastqsanger.gz
	SRR31677540.fastq.gz	Fastqsanger.gz
	SRR31677541.fastq.gz	Fastqsanger.gz
	SRR31677542.fastq.gz	Fastqsanger.gz
	SRR31677543.fastq.gz	Fastqsanger.gz

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Project description:ONT direct RNA sequencing of MCF7 cells upon E2 induction

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MAF Amplification licenses Estrogen Receptor α to Drive Breast Cancer Metastasis [RNA-seq]

Project description:We performed mRNA profiling of control and MAF-overexpressing MCF7 cells to assess the transcriptional consequences of estrogen receptor (ER) activation upon metastatic MAF expression. To this end, we cultured MCF7 cells in hormone-deprived (HD) medium for 72 h and then estrogen (E2) or vehicle was added for 6h prior to RNA extraction. Samples were generated in triplicate. We report that MAF supports the expression of genes involved in metastatic functions and that E2 treatment correlates with E2 early and late gene responses and cell cycle regulation. Additionally, a set of MAF and E2-dependent gene responses was identified. Our results show that MAF expression causes an expansion of ER-mediated transcriptional events in MCF7 cells exposed to E2. Additionally, we silenced KDM1A expression in MAF-overexpressing MCF7 cells to test whether this histone demethylase mediates the transcriptional consequences of MAF overexpression. Samples with KDM1A knockdown were generated in duplicates. We report that KDM1A partially regulates MAF/E2-dependent gene responses.

2023-09-15 | GSE210607 | GEO

MAF Amplification licenses Estrogen Receptor α to Drive Breast Cancer Metastasis [ER ChIP-seq]

Project description:We performed genome-wide mapping of estrogen receptor (ER) binding sites in control and MAF-overexpressing MCF7 cells to assess the consequences of estrogen (E2) stimulation upon metastasic MAF expression. To this end, we cultured MCF7 cells in hormone-deprived (HD) medium for 72 h and then E2 or vehicle was added for 1h prior to chromatin immunoprecipitation (ChIP). Samples were generated in triplicate. We report that E2 induces extensive ER recruitment to chromatin and that ER-binding is gained and expanded upon MAF overexpression.

2023-09-15 | GSE210604 | GEO

MAF Amplification licenses Estrogen Receptor α to Drive Breast Cancer Metastasis [dataset 1]

Project description:We performed mRNA profiling of control and MAF-overexpressing MCF7 cells to assess the transcriptional consequences of estrogen receptor (ER) activation upon metastatic MAF expression in the presence or absence or ER (using a protac for ER degradation). To this end, we cultured MCF7 cells in hormone-deprived (HD) medium for 72 h. At this point, we treated the cells with vehice or ER-protac for 24h and then estrogen (E2) or vehicle was added for 6h prior to RNA extraction. Samples were generated in triplicate. We report that MAF supports the expression of genes involved in metastatic functions and that E2 treatment and ER expression correlates with E2 early and late gene responses and cell cycle regulation. Additionally, a set of MAF and ER-dependent gene responses was identified. Our results show that MAF expression causes an expansion of ER-mediated transcriptional events in MCF7 cells exposed to E2.

2023-09-15 | GSE232175 | GEO

Regulation of TET2 gene expression and 5mC oxidation in breast cancer cells by estrogen signaling [hMeDIP-seq]

Project description:Estrogen signaling plays important roles in diverse physiological and pathophysiological processes. However, the relationship between estrogen signaling and epigenetic regulation is not fully understood. Here, we explored the effect of estrogen signaling on the expression of Ten-Eleven Translocation (TET) family genes and DNA hydroxylmethylation in estrogen receptor alpha positive (ERα+) breast cancer cells. By analyzing the RNA-seq data, we identified TET2 as an estradiol (E2)-responsive gene in ERα+ MCF7 cells. RT-qPCR and Western blot analyses confirmed that both the mRNA and protein levels of TET2 gene were upregulated in MCF7 cells by E2 treatment. ChIP-seq and qPCR analyses showed that the enrichment of ERα and H3K27ac on the upstream regulatory regions of TET2 gene was increased in MCF7 cells upon E2 treatment. Moreover, E2 treatment also led to a significant increase in the global 5-hydroxymethylcytosine (5hmC) level, while knockout of TET2 abolished such E2-induced 5hmC increase. Conversely, treatment with ICI 182780, a potent and selective estrogen receptor degrader (SERD), inhibited TET2 gene expression and down-regulated the 5hmC level in MCF7 cells. Taken together, our study identified an ERα/TET2/5hmC epigenetic pathway, which may participate in the estrogen-associated physiological and pathophysiological processes.

2021-11-28 | GSE189507 | GEO

Genome wide DRIP-seq in E2 stimulated MCF7 cells

Project description:We mapped the location of RNA-DNA hybrids in hormone-starved MCF7 breast cancer cells treated with the hormone estradiol (E2.) E2 is a potent transcriptional activator, and causes proliferation in hormone starved cells. We find a significant induction of hybrids at genes known to be regulated by the estrogen receptor.

2016-08-23 | GSE81851 | GEO

MAF Amplification licenses Estrogen Receptor α to Drive Breast Cancer Metastasis [MAF ChIP-seq]

Project description:We performed genome-wide mapping of MAF binding sites in control and MAF-overexpressing MCF7 cells to assess the consequences of estrogen (E2) stimulation on MAF recruitment to chromatin. To this end, we cultured MCF7 cells in hormone-deprived (HD) medium for 72 h and then E2 or vehicle was added for 1h prior to chromatin immunoprecipitation (ChIP). Samples were generated in triplicate. We report that MAF binding is largely independent of E2

2023-09-15 | GSE210605 | GEO

MAF Amplification licenses Estrogen Receptor α to Drive Breast Cancer Metastasis [ATAC-seq]

Project description:We mapped chromatin accessibility on control and MAF-overexpressing MCF7 cells to assess the consequences of estrogen (E2) and metastatic MAF expression on the chromatin landscape. To this end, we cultured MCF7 cells in hormone-deprived (HD) medium for 72 h and estrogen (E2) or vehicle was added for 1h prior to DNA purification. Samples were generated in quadruplicate. We report changes in chromaitn accessibility depending on both MAF expression and E2 stimulation.

2023-09-15 | GSE210603 | GEO

Proteomic Analysis Reveals the Major Proteins and Pathways that Mediate the Effect of 17-β-Estradiol in Cell Division and Apoptosis in Breast Cancer MCF7 Cells

Project description:Despite extensive research, the genes/proteins and biological pathways responsible for the physiological effects of estrogen remain elusive. In this study, we employed a proteomic method to determine the effect of estrogen on global protein expression in breast cancer MCF7 cells. The expression of 77 cytoplasmic, 74 nuclear, and 81 membrane proteins was significantly altered by 17-β-estradiol (E2). Protein enrichment analyses of the quantified proteins revealed that E2 stimulated cell division primarily by promoting the G1 to S phase transition and advancing the G2/M checkpoint. Functional annotation analyses of the E2-regulated proteins indicated that these proteins promoted cell division primarily through enhancing protein nuclear import, protein translation, reducing mRNA degradation, and increasing protein folding. Interestingly, many of the E2-upregulated proteins contained the HEAT, KH, and RRM domains. The effect of E2 on cell survival was complex, as it could simultaneously enhance and inhibit apoptosis. E2 enhanced apoptosis by promoting cytochrome c release from mitochondria and inhibited apoptosis by activating the PI3K/AKT/mTOR signaling pathway. Treatment of MCF7 cells with E2 and the PI3K inhibitor Ly294002 significantly enhanced apoptosis compared to the cells treated with E2 alone. Our results suggest that combining estrogen with a PI3K inhibitor could be a promising strategy for treating ERα-positive breast cancer.

2025-05-06 | PXD049343 | Pride

Temporal dynamic reorganization of 3D chromatin in hormone-induced breast cancer and endocrine resistance

Project description:To establish a data-driven learning model of the temporal dynamics and 3D chromatin reorganization, we conducted tethered chromatin conformation (TCC) sequencing to examine 3D structure dynamics in estradiol (E2)-induced breast cancer MCF7 cells and Tamoxifen resistant breast cancer MCF7 cells.

2019-04-09 | GSE108787 | GEO

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