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AP-2β activates enhancers that define mammary hormone sensing cell identity [ChIP-Seq]

ABSTRACT: AP-2β activates enhancers that define mammary hormone sensing cell identity [ChIP-Seq]

PROVIDER: PRJNA854196 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19903600.fastq.gz	Fastqsanger.gz
	SRR19903601.fastq.gz	Fastqsanger.gz
	SRR19903602.fastq.gz	Fastqsanger.gz
	SRR19903603.fastq.gz	Fastqsanger.gz
	SRR19903604.fastq.gz	Fastqsanger.gz

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AP-2β activates enhancers that define mammary hormone sensing cell identity

Project description:AP-2β activates enhancers that define mammary hormone sensing cell identity

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AP-2β activates enhancers that define mammary hormone sensing cell identity [ChIP-Seq]

Project description:The Activating Protein 2β transcription factor (TFAP2B; AP-2β) is a marker for both lobular and molecular apocrine/HER2-E breast cancers, despite these tumours having very different prognoses. We show that simultaneous expression of both AP-2β and the estrogen receptor (ESR1, ER) marks well differentiated, low proliferation cells that are characteristic of luminal A lobular tumours, but loss of ER expression occurs when the tumour cells progress to molecular apocrine tumours. To discover potential explanations for this behaviour we performed chromatin immunoprecipitation sequencing (ChIP-seq) for AP-2β, AR, GATA3, FOXA1 and H3K27 acetylation in ER-negative MDA-MB-453 breast cancer cells. We find that all four transcription factors frequently bind to the same enhancers and that these enhancers are more likely to be active when AP-2β is present. Molecular apocrine genes are significantly more likely to have enhancers bound to all four transcription factors flanked by H3K27 acetylation. When AP-2β binds separately from the other factors, it binds close to the transcription start site, where it shows very high enrichment for H3K27 acetylation. AP-2 family proteins activate transcription by recruiting CITED proteins and p300/CBP. Since AR, FOXA1 and GATA3 are themselves able to recruit histone acetyl-transferases, we infer that AP-2β regulates the activity of those histone acetyl-transferases. We propose that this broad fundamental role in transcription explains the contradictory functions, both oncogenic and tumour suppressing, that have been assigned to AP-2 family members in previous studies on cancer.

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AP-2β activates enhancers that define mammary hormone sensing cell identity [RNA-seq]

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Project description:AP-2β activates enhancers that define mammary hormone sensing cell identity [RNA-seq]

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AP-2β activates enhancers that define mammary hormone sensing cell identity

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AP-2α and AP-2β cooperatively orchestrate homeobox gene expression during branchial arch patterning

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Project description:Recent development of new immune checkpoint inhibitors has been particularly successfully in cancer treatment, but still the majority patients fail to benefit. Converting resistant tumors to immunotherapy sensitivity will provide a significant improvement in patient outcome. Here we identify Mi-2β as a key melanoma-intrinsic effector regulating the adaptive anti-tumor immune response. Genetically engineered mouse melanoma studies indicate that loss of Mi-2β rescued the immune response to immunotherapy in vivo. Mechanistically, ATAC-seq indicate that Mi-2β controlled the accessibility of IFN-γ-stimulated genes (ISGs). Mi-2β bound to EZH2 and promote K510 methylation of EZH2 and subsequently activate the trimethylation of H3K27 to inhibit the transcription of ISGs. Finally, we develop an Mi-2β-targeted inhibitor, Z36-MP5, which targeted inhibition of Mi-2β ATPase activity and recovered ISG transcription. Consequently, Z36-MP5 efficiently induce a response to immunotherapy in otherwise resistant melanomas. Our work provides a potential therapeutic strategy to convert immunotherapy resistant melanomas to sensitive ones.

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Functional interactions between Mi-2β and AP1 complexes control response and recovery from barrier disruption

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