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27 Hydroxycholesterol represses G9a expression via Estrogen Receptor alpha in breast cancer

ABSTRACT: 27 Hydroxycholesterol represses G9a expression via Estrogen Receptor alpha in breast cancer

PROVIDER: PRJNA974381 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24658115.fastq.gz	Fastqsanger.gz
	SRR24658116.fastq.gz	Fastqsanger.gz
	SRR24658117.fastq.gz	Fastqsanger.gz

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27 Hydroxycholesterol represses G9a expression via Estrogen Receptor alpha in breast cancer

Project description:ChIP-sequencing for the H3K9me2 mark in MCF-7 cells showed that 27-HC treatment reduces the H3K9me2 mark on subset of genes linked to cancer progression, proliferation, and metastasis

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Regulation of 27-hydroxycholesterol metabolism by ZMYND8

Project description:ZMYND8 is a master regulator of 27-hydroxycholesterol metabolism in breast cancer stem cells.

2022-06-02 | GSE186543 | GEO

Macrophage-to-endothelial Cell Crosstalk by 27-hydroxycholesterol Promotes Atherosclerosis in Male Mice

Project description:Human aortic endothelial cells were treated with vehicle (LUM1_S07615), estradiol (LUM1_S07617) or 27-hydroxycholesterol (LUM1_S07618), estrogen receptor alpha was immunoprecipitated, and the changes in the receptor interactome were interrogated.

2023-05-08 | MSV000091880 | MassIVE

Regulation of 27-hydroxycholesterol metabolism by ZMYND8 in mammospheres

Project description:ZMYND8 is a master regulator of 27-hydroxycholesterol metabolism in breast cancer stem cells.

2022-06-02 | GSE203054 | GEO

27-Hydroxycholesterol links cholesterol and breast cancer pathophysiology.

Project description:The cholesterol metabolite and SERM, 27HC, is the signaling molecule that links cholesterol to breast cancer pathophysiology Hypercholesterolemia is a risk factor for breast cancer, and patients taking statins demonstrate lower breast cancer incidence and decreased breast cancer recurrence, data that highlights the potential importance of the recent finding that 27-Hydroxycholesterol (27HC), a primary metabolite of cholesterol, acts as a selective estrogen receptor modulator (SERM). The goal of this study was to evaluate the impact of 27HC on breast cancer pathophysiology. Elevation of 27HC in murine models increased tumor growth in an estrogen receptor dependent manner. Importantly, a high cholesterol diet decreased the time to tumor onset and increased tumor growth, and this response required presence of CYP27A1. Within human breast cancer samples, CYP27A1 expression increasesd with grade, in addition to being highly expressed in tumor associated macrophages. Finally 27HC increases metastasis to the lung. The findings herein strongly support a role for 27HC in breast cancer pathophysiology, providing support for the exploration of potential chemopreventative benefits of lower cholesterol diets, and pharmacological inhibitors of HMG-CoA reductase or CYP27A1. MCF-7 cells were treated as indicated in the presence of E2 or vehicle; RNA was isolated and used for preparation of label for 3' expression analysis.

2013-08-01 | E-GEOD-46924 | biostudies-arrayexpress

27-Hydroxycholesterol represses G9a expression via oestrogen receptor alpha in breast cancer.

Project description:27-hydroxycholesterol (27-HC) is a cholesterol metabolite and the first discovered endogenous selective estrogen receptor modulator (SERM) that has been shown to have proliferative and metastatic activity in breast cancer. However, whether 27-HC metabolite modulates the epigenetic signatures in breast cancer and its progression remains unclear. The current study, reports that 27-HC represses the expression of euchromatic histone lysine methyltransferase G9a, further reducing di-methylation at H3K9 in a subset of genes. We also observed reduced occupancy of ERα at the G9a promoter, indicating that 27-HC negatively regulates the ERα occupancy on the G9a promoter and functions as a transcriptional repressor. Further, ChIP-sequencing for the H3K9me2 mark has demonstrated that 27-HC treatment reduces the H3K9me2 mark on subset of genes linked to cancer progression, proliferation, and metastasis. We observed upregulation of these genes following 27-HC treatment which further confirms the loss of methylation at these genes. Immunohistochemical analysis with breast cancer patient tissues indicated a positive correlation between G9a expression and CYP7B1, a key enzyme of 27-HC catabolism. Overall, this study reports that 27-HC represses G9a expression via ERα and reduces the levels of H3K9me2 on a subset of genes, including the genes that aid in breast tumorigenesis and invasion further, increasing its expression in the breast cancer cells.

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Regulation of 27-hydroxycholesterol metabolism by ZMYND8

Project description:Regulation of 27-hydroxycholesterol metabolism by ZMYND8

| PRJNA774341 | ENA

27-Hydroxycholesterol links cholesterol and breast cancer pathophysiology.

2013-08-01 | GSE46924 | GEO

Histone H3K9 Methyltransferase G9a Represses PPARγ Expression and Adipogenesis [Affymetrix expression data]

Project description:PPARγ promotes adipogenesis while Wnt proteins inhibit adipogenesis. However, the mechanisms that control expression of these positive and negative master regulators of adipogenesis remain incompletely understood. By genome-wide histone methylation profiling in preadipocytes, we find that among gene loci encoding adipogenesis regulators, histone methyltransferase (HMT) G9a-mediated repressive epigenetic mark H3K9me2 is enriched on the entire PPARγ locus. H3K9me2 and G9a levels decrease during adipogenesis, which correlates inversely with induction of PPARγ. Removal of H3K9me2 by G9a deletion enhances chromatin opening and binding of adipogenic transcription factor C/EBP-beta to PPARγ promoter, which promotes PPARγ expression. Interestingly, G9a represses PPARγ expression in an HMT activity-dependent manner but facilitates Wnt10a expression independent of its enzymatic activity. Consistently, deletion of G9a or inhibiting G9a HMT activity promotes adipogenesis. Finally, deletion of G9a in mouse adipose tissues increases adipogenic gene expression and tissue weight. Thus, by inhibiting PPARγ expression and facilitating Wnt10a expression, G9a represses adipogenesis. Examination of gene expression changes in G9a KO brown preadipocytes

2013-02-01 | E-GEOD-41456 | biostudies-arrayexpress

G9a selectively represses a class of late-replicating genes at the nuclear periphery

Project description:This SuperSeries is composed of the following subset Series: GSE18076: G9a selectively represses a class of late-replicating genes at the nuclear periphery (Expression) GSE18079: G9a selectively represses a class of late-replicating genes at the nuclear periphery (WG_CGH) Refer to individual Series

2009-11-02 | E-GEOD-18082 | biostudies-arrayexpress

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