Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Regulation of 27-hydroxycholesterol metabolism by ZMYND8 in mammospheres

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

ORGANISM(S): Homo sapiens

PROVIDER: GSE203054 | GEO | 2022/06/02

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

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

Regulation of 27-hydroxycholesterol metabolism by ZMYND8 in mammospheres

Project description:Regulation of 27-hydroxycholesterol metabolism by ZMYND8 in mammospheres

| PRJNA838362 | ENA

Regulation of 27-hydroxycholesterol metabolism by ZMYND8

Project description:Regulation of 27-hydroxycholesterol metabolism by ZMYND8

| PRJNA774341 | ENA

The cholesterol metabolite 27-hydroxycholesterol increases the secretion of extracellular vesicles which promote breast cancer progression

Project description:Mice bearing Met1 tumors were treated with extracellular vessicles (EVs) isolated from neutrophils treated with vehicle (DMSO) or 27-hydroxycholesterol. RNAseq was performed on harvested tumors.

2021-06-16 | GSE171949 | 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

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

27-Hydroxycholesterol links cholesterol and breast cancer pathophysiology.

2013-08-01 | GSE46924 | GEO

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

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

| PRJNA974381 | ENA

ZMYND8 is a master regulator of 27-hydroxycholesterol that promotes tumorigenicity of breast cancer stem cells.

Project description:27-Hydroxycholesterol (27-HC) is the most abundant oxysterol that increases the risk of breast cancer progression. However, little is known about epigenetic regulation of 27-HC metabolism and its role in breast tumor initiation. Using genetic mouse mammary tumor and human breast cancer models, we showed here that the histone reader ZMYND8 was selectively expressed in breast cancer stem cells (BCSCs) and promoted epithelial-mesenchymal transition (EMT), BCSC maintenance and self-renewal, and oncogenic transformation through its epigenetic functions, leading to breast tumor initiation. Mechanistically, ZMYND8 was a master transcriptional regulator of 27-HC metabolism. It increased cholesterol biosynthesis and oxidation but blocked cholesterol efflux and 27-HC catabolism, leading to accumulation of 27-HC in BCSCs. Consequently, 27-HC promoted EMT, oncogenic transformation, and tumor initiation through activation of liver X receptor. These findings reveal that ZMYND8 is an epigenetic booster that drives breast tumor initiation through metabolic reprogramming.

| S-EPMC9286501 | biostudies-literature

ZMYND8 reads the dual histone mark H3K4me1-H3K14ac to antagonize the expression of metastasis-linked genes

Project description:Histone acetylation, including acetylated H3K14 (H3K14ac), is generally linked to gene activation. Monomethylated histone H3 lysine 4 (H3K4me1), together with other gene-activating marks, denotes active genes. In contrast to usual gene-activating functions of H3K14ac and H3K4me1, we here show that the dual histone modification mark H3K4me1-H3K14ac is recognized by ZMYND8 (also called RACK7) and functions to counteract gene expression. We identified ZMYND8 as a transcriptional corepressor of the H3K4 demethylase JARID1D. ZMYND8 antagonizes the expression of metastasis-linked genes, and its knockdown increases the cellular invasiveness in vitro and in vivo. The plant homeodomain (PHD) and Bromodomain cassette in ZMYND8 mediates the combinatorial recognition of H3K4me1-H3K14ac and H3K4me0-H3K14ac by ZMYND8. These findings uncover an unexpected role for the signature H3K4me1-H3K14ac in attenuating gene expression and reveal a previously unknown metastasis-suppressive epigenetic mechanism in which ZMYND8's PHD-Bromo cassette couples H3K4me1-H3K14ac with repression of metastasis-linked genes. i) ChIP-Seq data of ZMYND8, JARID1D, H3K4me1, H3K14ac, H3K4me3, and H3K27me3 in normal DU145 cells. ii) ChIP-Seq data of H3K4me1 and H3K4me3 in shLuciferase-, shJARID1D-, or shZMYND8-treated DU145 cells. iii) RNA-Seq data in shLuciferase-, shJARID1D-, or shZMYND8-treated DU145 cells.

2016-07-28 | E-GEOD-82260 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data