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SETD7 functions as a transcription repressor in prostate cancer via methylating FOXA1 [RNA-seq]

ABSTRACT: SETD7 functions as a transcription repressor in prostate cancer via methylating FOXA1 [RNA-seq]

PROVIDER: PRJNA902336 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22311712.fastq.gz	Fastqsanger.gz
	SRR22311713.fastq.gz	Fastqsanger.gz
	SRR22311714.fastq.gz	Fastqsanger.gz
	SRR22311715.fastq.gz	Fastqsanger.gz
	SRR22311716_1.fastq.gz	Fastqsanger.gz

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SETD7 functions as a transcription repressor in prostate cancer via methylating FOXA1 [ChIP-seq]

Project description:We recently reported that in prostate cancer LSD1 can demethylate the lysine 270 of FOXA1 to stabilize FOXA1 chromatin binding and thus can enhance the activities of AR and other transcription factors that require FOXA1 as a pioneer factor. However, the methyltransferase that can methylate FOXA1 and negatively regulate the LSD1-FOXA1 oncogenic axis remains unknown. SETD7 is initially identified as a transcriptional activator through methylating histone 3 lysine 4 but can also function as a methyltransferase on other non-histone substrates. However, its function in PCa remains poorly understood. In this study, we found that SETD7 confers tumor suppressor activity in PCa cells and that loss of SETD7 expression is significantly associated with PCa progression and tumor aggressiveness. Mechanistically, we found that SETD7 primarily acts as a transcriptional repressor in CRPC cells by functioning as a methyltransferase of FOXA1-K270 to disrupt FOXA1-mediated transcription. Overall, our study provides novel mechanistic insights into the tumor-suppressive and transcriptional repression activities of SETD7 in mediating PCa progression and therapy resistance.

2023-08-23 | GSE218092 | GEO

SETD7 functions as a transcription repressor in prostate cancer via methylating FOXA1

Project description:SETD7 functions as a transcription repressor in prostate cancer via methylating FOXA1

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SETD7 functions as a transcription repressor in prostate cancer via methylating FOXA1 [ChIP-seq]

Project description:SETD7 functions as a transcription repressor in prostate cancer via methylating FOXA1 [ChIP-seq]

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SETD7 functions as a transcription repressor in prostate cancer via methylating FOXA1 [RNA-seq]

Project description:To determine the transcriptional impact of SETD7,MLL1 silencing in CRPC cells, we performed an RNA-seq analysis in those 22Rv1 stable cell lines (under hormone-depleted conditions)

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SETD7 functions as a transcription repressor in prostate cancer via methylating FOXA1

Project description:This SuperSeries is composed of the SubSeries listed below.

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Essential Roles of SETD7 as Transcriptional Activator and Co-regulator of H3K36me in Cardiac Lineage Commitment

Project description:Coordinated epigenome alteration is fundamental for cardiac development. However, the precise mechanisms by which epigenetic modifying enzymes regulate cardiac development are still unclear. Here we identify SET domain containing protein 7 (SETD7) as a key regulator of cardiac differentiation. ChIP-seq reveals that SETD7 has distinct groups of target genes and regulates its stage-specific expression during cardiomyocyte differentiation, which is crucial for lineage commitment. We find SETD7 associates with stage-specific co-factors, such as SWI/SNF chromatin remodeling factors during mesodermal formation and transcription factor NKX2-5 in cardiac progenitor differentiation. Cross-analysis of epigenetic modifications shows that SETD7 recognizes and binds with active histone marker H3K36 methylation on gene-body region of its target genes. We further demonstrate SETD7 is required for functional properties of terminally differentiated cardiomyocytes. Together, our results suggest unidentified roles of SETD7 in cardiac lineage commitment and provide new insights into the crosstalk between epigenetic dynamics and epigenetic modifying enzymes.

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FOXA1 O-GlcNAcylation-mediated transcriptional switch governs metastasis capacity in breast cancer [RNA-seq]

Project description:The transcription factor FOXA1, which functions in epigenetic reprogramming, plays a critical role in breast cancer progression. However, the molecular mechanisms by which FOXA1 achieves its oncogenic functions remain elusive. Here, we demonstrate that the O-GlcNAcylation of FOXA1 increases breast cancer metastasis capacity by orchestrating the transcription of numerous metastasis regulators. O-GlcNAcylation at Thr432, Ser441 and Ser443 regulates the stability of FOXA1 and promotes its assembly with chromatin in breast cancer cells. We provide evidence that O-GlcNAcylation shapes the FOXA1 interactome, especially triggering the recruitment of the transcriptional repressor MECP2 and consequently stimulating FOXA1 chromatin-binding sites to switch to chromatin loci of adhesion-related genes, including EPB41L3 and COL9A2. Site-specific depletion of O-GlcNAcylation on FOXA1 affects the expression of various downstream genes and thus inhibits breast cancer proliferation and metastasis both in vitro and in vivo.

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FOXA1 O-GlcNAcylation-mediated transcriptional switch governs metastasis capacity in breast cancer [ChIP-seq]

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