Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA101033 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:human prostate and breast epithelial cell lines with EZH2 siRNA interference
| PRJNA101035 | ENA
Project description:Transcriptional profiling of human prostate and breast epithelial cells with a time course analysis of EZH2 overexpression of cells at 3, 6, 12, 24, 48, and 72 hrs respectively. Keywords: Genetic modification
2007-11-01 | GSE8144 | GEO
Project description:Transcriptional profiling of human prostate and breast epithelial cells comparing control siRNA-treated with EZH2-siRNA treated Keywords: Genetic modification
2007-11-01 | GSE8145 | GEO
Project description:Study of the transcriptome changes upon Hotair overexpression in wt and Ezh2-/- Human breast cancer cell lines
2016-08-12 | GSE72524 | GEO
Project description:Overexpression of EZH2 in estrogen receptor negative (ER-) breast cancer promotes metastasis. EZH2 has been mainly studied as the catalytic component of the Polycomb Repressive Complex 2 (PRC2) that mediates gene repression by trimethylating histone H3 at lysine 27 (H3K27me3). However, how EZH2 drives metastasis despite the low H3K27me3 levels observed in ER- breast cancer is unknown. We have shown that in human invasive carcinomas and distant metastases, cytoplasmic EZH2 phosphorylated at T367 is significantly associated with ER- disease and low H3K27me3 levels. Here, we explore the interactome of EZH2 and of a phosphodeficient mutant EZH2_T367A. We identified novel interactors of EZH2, and identified interactions that are dependent on the phosphorylation and cellular localization of EZH2 that may play a role in EZH2 dependent metastatic progression.
2018-07-03 | PXD010073 | Pride
Project description:Genome-wide analysis of human prostate epithelial cell lines
| PRJNA288468 | ENA
Project description:It is well established that EZH2, a lysine methyltransferase, is upregulated in most of aggressive cancers, highlighting the importance of EZH2 in cancer progression. Recent research has shown that metabolic reprogramming is pivotal in various biological processes, including cancer. Despite this, evidence of EZH2's role in regulating cancer metabolism remains limited. Our study reveals a negative correlation between EZH2 and HMGCS2, a gene belongs to the HMG-CoA synthase, in prostate and breast cancers. Furthermore, HMGCS2 is inversely related to cancer progression and prognosis in these cancers and is epigenetically repressed by EZH2 both in vitro and in vivo. Notably, restored EZH2 reduces the elevated HMGCS2 levels observed upon EZH2 depletion. Overexpression of HMGCS2 decreases tumorigenesis in both prostate and breast cancers. Additionally, β-hydroxybutyrate (BHB), a downstream metabolite of HMGCS2, impedes prostate cancer progression by targeting EZH2 via direct protein-compound interaction -mediated protein degradation. More importantly, ketone drink of BHB administration dramatically reduces tumor size and weight in a prostate cancer xenograft model. Combining ketone drink with FDA-approved drugs enzalutamide and Tazemetostat further suppresses tumor progression. Overall, EZH2- HMGCS2-BHB regulatory network plays a critical role in the progression of prostate cancer and ketone drink is a novel therapeutic tool for patients with aggressive prostate cancer.
2025-05-27 | GSE269259 | GEO
Project description:It is well established that EZH2, a lysine methyltransferase, is upregulated in most of aggressive cancers, highlighting the importance of EZH2 in cancer progression. Recent research has shown that metabolic reprogramming is pivotal in various biological processes, including cancer. Despite this, evidence of EZH2's role in regulating cancer metabolism remains limited. Our study reveals a negative correlation between EZH2 and HMGCS2, a gene belongs to the HMG-CoA synthase, in prostate and breast cancers. Furthermore, HMGCS2 is inversely related to cancer progression and prognosis in these cancers and is epigenetically repressed by EZH2 both in vitro and in vivo. Notably, restored EZH2 reduces the elevated HMGCS2 levels observed upon EZH2 depletion. Overexpression of HMGCS2 decreases tumorigenesis in both prostate and breast cancers. Additionally, β-hydroxybutyrate (BHB), a downstream metabolite of HMGCS2, impedes prostate cancer progression by targeting EZH2 via direct protein-compound interaction -mediated protein degradation. More importantly, ketone drink of BHB administration dramatically reduces tumor size and weight in a prostate cancer xenograft model. Combining ketone drink with FDA-approved drugs enzalutamide and Tazemetostat further suppresses tumor progression. Overall, EZH2- HMGCS2-BHB regulatory network plays a critical role in the progression of prostate cancer and ketone drink is a novel therapeutic tool for patients with aggressive prostate cancer.
2025-05-27 | GSE269208 | GEO
Project description:To determine the altered mRNA expression signatures upon overexpressing EZH2 regulated microRNAs in cancer. To identify EZH2 regulated microRNAs in cancer. Two-condition experiment: Each EZH2 microRNA was overexpressed and compared to a control RNA in BT549 breast cancer cells. In DU145 prostate cancer cell EZH2 was knocked down and comapred to EZH2 scrambled siRNA. Other cell lines were monitored for miRNA expression as they are known to have high endogenous levels of EZH2.
2011-10-20 | E-GEOD-26996 | biostudies-arrayexpress
Project description:<p>BRCA1 mutations are a hallmark of hereditary ovarian cancer, strongly linked to deficiencies in homologous recombination (HR) DNA repair and impaired DNA replication fork protection. However, its roles in cancer progression beyond maintaining genomic integrity remain poorly understood. Through metabolomics approaches, we found BRCA1-deficiency strikingly increased choline metabolism. Loss of BRCA1 promotes choline uptake through upregulating choline transporter-like protein 4 (CTL4). BRCA1 directly binds and recruits EZH2-mediated H3K27Me3 deposition to CTL4 promoter. CTL4 was therefore overexpressed in ovarian cancer tissues with BRCA1 mutations. Furthermore, BRCA1-deficiency significantly promotes ovarian cancer invasion, while inhibition of CTL4 reverses the high metastatic potential of BRCA1-deficient ovarian cancer cells, suggesting the functionality and specificity of CTL4 as a therapeutic target. Additionally, we discovered that phosphocholine, the choline metabolite increased by CTL4 overexpression, interacted with and stabilized the epithelial-to-mesenchymal transition inducer FAM3C in BRCA1-deficient ovarian cancer cells. Importantly, we identified a potent CTL4 inhibitor, DT-13, which significantly reduces choline metabolism and effectively suppresses metastasis in BRCA1-deficient ovarian cancers. Therefore, our study uncovers a mechanism underlying metastasis in BRCA1-deficient cancers and identifies CTL4 as a therapeutic target for metastatic ovarian cancer patients with BRCA1 mutations.</p>
2026-05-15 | MTBLS12245 | MetaboLights