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Genome-wide Profiling of H3K27ac binding in human MCF-7 cell lines

ABSTRACT: Genome-wide Profiling of H3K27ac binding in human MCF-7 cell lines

PROVIDER: PRJNA549608 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9326373.fastq.gz	Fastqsanger.gz
	SRR9326374.fastq.gz	Fastqsanger.gz
	SRR9326375.fastq.gz	Fastqsanger.gz

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Genome-wide Profiling of H3K27ac binding in human cancer cell lines

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Genome-wide Profiling of H3K27ac binding in human cancer cell lines

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Genome-wide Profiling of H3K27ac binding in human MCF-7 cell lines

Project description:The histone methyltransferase EZH2 has been shown to function as a multifaceted molecule which can switch from a transcriptional repressor to an activator inducing a subset of genes that promote oncogenesis, including breast cancer. TfR-1, a key mediator in iron absorption, is highly expressed in a variety of tumors and associated with tumor grade, tumor stage and prognosis of patients. However, the known regulation mechanism of TfR-1 mainly remains on post-transcriptional level. To figure out whether TfR-1 expression is under epigenetic control, we examined the influence of EZH2 depletion and inhibition on TfR-1 expression in different subtypes of breast cancer cells. We discovered that EZH2 context-dependently modulates TfR-1 level and manipulates cellular iron uptake. Moreover, we identified TfR-1 as an NF-κB target gene which is positively regulated by EZH2 via constructing a complex with p65-p50 and transcription factor AP-1 in ER- cells. Inversely, TfR-1 is repressed by EZH2 and ER through histone methylation on its promoter in ER+ cells. These ﬁndings demonstrated an additional role of EZH2 in promoting breast cancer progression through iron homeostasis regulation and underscore the need for developing context-speciﬁc strategy for therapeutic targeting of epigenetic inhibition in breast cancer.

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