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Transcriptional regulation in MCF-7 breast cancer cells treated with proteasome inhibitor MG132 [rna_polii_chIP-seq]

ABSTRACT: Transcriptional regulation in MCF-7 breast cancer cells treated with proteasome inhibitor MG132 [rna_polii_chIP-seq]

PROVIDER: PRJNA595566 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10691026_1.fastq.gz	Fastqsanger.gz
	SRR10691026_2.fastq.gz	Fastqsanger.gz
	SRR10691027_1.fastq.gz	Fastqsanger.gz
	SRR10691027_2.fastq.gz	Fastqsanger.gz
	SRR10691028_1.fastq.gz	Fastqsanger.gz

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Chromatin state of MCF-7 breast cancer cells treated with proteasome inhibitor MG132 [histone_mod_chip_seq]

Project description:We report whole genome chromatin immunoprecipitation followed by sequencing (ChIP-seq) of histone modifications in MCF-7 breast cancer cells treated with vehicle (UNTR) or the proteasome inhibitor MG132 for 4 (MG4H) or 24 (MG24H) hours. We find that MG132 treatment results in the spreading of the H3-trimethyl lysine 4 mark into gene bodies of a subset of induced genes in MCF-7 cells. The spreading of the H3K4me3 is concomitant with hyperacetylation (H3K27ac, K122ac and K9/14ac) of the corresponding gene TSS. H3 Lysine 36 trimethylation mark is enriched at genes that are induced by MG132. Finally, we show that proteasome inhibition establishes a chromatin state that enhances antiproliferative, while dampening cell proliferative gene expression programs relevant to breast cancer. The study provides a comprehensive resource of histone modifications in proteasome inhibited cells.

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Transcriptional regulation in MCF-7 breast cancer cells treated with proteasome inhibitor MG132 [rna_polii_chIP-seq]

Project description:We report whole genome chromatin immunoprecipitation followed by sequencing (ChIP-seq) of 3 different RNA Pol II CTD modifications in MCF-7 breast cancer cells treated with vehicle (UNTR) or the proteasome inhibitor MG132 for 4 (MG4H) or 24 (MG24H) hours. We find the non-phosphorylated form of RNA Pol II CTD accumulates at TSS of all expressed genes in proteasome inhibited cells, particularly after 24H of MG132 treatment. Proteasome inhibition enhances Ser5-P and Ser2-P binding at TSS of genes induced by MG132. We note that proteasome inhibition establishes unique Ser2-P 5’ to 3’ gene profiles at induced compared to repressed genes. Overall proteasome inhibition enhances RNA Pol II processivity and expression of gene networks relevant to breast cancer. The study provides a comprehensive resource of RNA Pol II binding in proteasome inhibited cells.

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Project description:The objective of the study was to investigate the effect of proteasome inhibition on glucocorticoid and estrogen receptor regulated gene expression. Experiment Overall Design: MCF-7 cells were treated with proteasome inhibitor (MG132), dexamethasone, 17b-estradiol or MG132 plus dexamethasone or MG132 plus 7b-estardiol. Control cells were not treated. RNA was collected from 2 biological experiments.

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Chromatin state of MCF-7 breast cancer cells treated with proteasome inhibitor MG132 [histone_mod_chip_seq]

Project description:Chromatin state of MCF-7 breast cancer cells treated with proteasome inhibitor MG132 [histone_mod_chip_seq]

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Project description:Chromatin state and Transcriptional regulation in MCF-7 breast cancer cells treated with proteasome inhibitor MG132

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