Transcriptomic profiling of HepG2 cells upon EZH2 knockdown
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE312184 | GEO | 2026/05/12
REPOSITORIES: GEO
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Project description:This RNA-seq dataset was generated to investigate transcriptomic alteriations associated with hepatocellular carcinoma(HCC) progression and the functional role of EZH2 expression. Liver tissue samples were collected from normal controls, HCC patients with low EZH2 expression, and HCC patients with high EZH2 expression. Differential gene expression analysis confirmed a marked increase in EZH2 expression in HCC relative to normal tissues and revealed transcriptional programs associated with proliferative and metastatic characterisrics that were progressively enhanced according to EZH2 expression level. This dataset enables the exploration of EZH2-associated molecular signatures and their relevance to HCC malignancy and metastatic progression.
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2026-02-22 | GSE298836 | GEO
Project description:The roles of epigenetic regulator Ezh2 in TAMs of liver cancer still unclear. In this study, our results demonstrated that the absence of Ezh2 in bone marrow-derived macrophages (BMDMs) exacerbated M2-like phenotypic changes upon incubation with conditioned media (CM) from hepatocellular carcinoma (HCC) cell line Hepa1-6. The ATAC-seq revealed that the promoter regions of pyruvate metabolic process-related genes were more accessible in treated BMDMs Ezh2 KO.
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Project description:The molecular mechanisms of carcinogenesis have been deeply studied benefit from the highly developing biotechnologies. Here we used high throughput sequencing method to capture the global binding profiles on RNA and DNA of EZH2 and JARID2 in liver normal (THLE-2) and carcinoma (HepG2) cells, respectively. We found that EZH2 and JARID2 showed distinct binding profile in HepG2 and THLE-2 cells. By binding to the primary RNAs, bound transcripts of EZH2 and JARID2 in HepG2 showed significantly increased transcriptional level in hepatocellular carcinoma (HCC) patients. They bound transcripts were also highly related to the HCC development by performing gene set enrichment analysis (GSEA). By exploring the DNA binding profile, we also detected similar phenomena that EZH2 could increase the transcriptional level of bound genes in HepG2 cells, showing PRC2-independent functions in liver cancer cells. Integrating analysis of the RNA and DNA binding profile showed EZH2 could independent function at the transcriptional and post-transcriptional stages. In summary, we proposed that the novel regulatory functions of EZH2 and JARID2 that may promote the cancer development in carcinoma liver cells.
2022-07-04 | GSE133982 | GEO
Project description:The molecular mechanisms of carcinogenesis have been deeply studied benefit from the highly developing biotechnologies. Here we used high throughput sequencing method to capture the global binding profiles on RNA and DNA of EZH2 and JARID2 in liver normal (THLE-2) and carcinoma (HepG2) cells, respectively. We found that EZH2 and JARID2 showed distinct binding profile in HepG2 and THLE-2 cells. By binding to the primary RNAs, bound transcripts of EZH2 and JARID2 in HepG2 showed significantly increased transcriptional level in hepatocellular carcinoma (HCC) patients. They bound transcripts were also highly related to the HCC development by performing gene set enrichment analysis (GSEA). By exploring the DNA binding profile, we also detected similar phenomena that EZH2 could increase the transcriptional level of bound genes in HepG2 cells, showing PRC2-independent functions in liver cancer cells. Integrating analysis of the RNA and DNA binding profile showed EZH2 could independent function at the transcriptional and post-transcriptional stages. In summary, we proposed that the novel regulatory functions of EZH2 and JARID2 that may promote the cancer development in carcinoma liver cells.
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Project description:Epigenetic dysregulation is closely associated with the pathogenesis of hepatocellular carcinoma (HCC). Enhancer of zeste homolog 2 (EZH2) is a key protein involved in the exacerbation of various cancers, including HCC. Despite several clinical trials of epigenetic therapies targeting EZH2, the mechanisms underlying EZH2-mediated gene suppression in HCC are not fully understood. In this study, we investigated EZH2-mediated transcriptional programs under EZH2-selective inhibition through an integrative analysis of epigenomic (ATAC-seq) and transcriptomic (RNA-seq) approaches. To determine the impact of EZH2 dysfunction, we measured the levels of H3K27me3 and EZH2 expression using flow cytometry and reverse transcription quantitative real-time PCR (RT-qPCR), respectively. Notably, we found that higher expression of EZH2 was significantly correlated with poorer survival among HCC patients by reanalyzing transcriptomes in the cancer genome atlas (TCGA). Inhibition of EZH2 with Tazemetostat (EPZ-6438), a selective inhibitor of EZH2, showed that EZH2 regulates genes involved in lipid homeostasis, and cysteine-methionine metabolism. Among the 13 EZH2 target genes identified by transcriptomic and epigenomic profiling, we selected BHMT and CDO1, which were significantly associated with poor survival in HCC patients. When HCC cells were treated with Tazemetostat, the expression levels of the BHMT and CDO1 genes increased, while the expression levels of ferroptosis marker genes, such as FSP1, NFS1, and SLC7A11, decreased. This suggests that inhibiting EZH2 may have potential therapeutic benefits in HCC by regulating the expression of genes involved in important biological processes. Our study suggests that EZH2 epigenetically regulates ferroptosis by controlling cysteine metabolism in HCC.
2024-10-25 | GSE268195 | GEO
Project description:Epigenetic dysregulation is closely associated with the pathogenesis of hepatocellular carcinoma (HCC). Enhancer of zeste homolog 2 (EZH2) is a key protein involved in the exacerbation of various cancers, including HCC. Despite several clinical trials of epigenetic therapies targeting EZH2, the mechanisms underlying EZH2-mediated gene suppression in HCC are not fully understood. In this study, we investigated EZH2-mediated transcriptional programs under EZH2-selective inhibition through an integrative analysis of epigenomic (ATAC-seq) and transcriptomic (RNA-seq) approaches. To determine the impact of EZH2 dysfunction, we measured the levels of H3K27me3 and EZH2 expression using flow cytometry and reverse transcription quantitative real-time PCR (RT-qPCR), respectively. Notably, we found that higher expression of EZH2 was significantly correlated with poorer survival among HCC patients by reanalyzing transcriptomes in the cancer genome atlas (TCGA). Inhibition of EZH2 with Tazemetostat (EPZ-6438), a selective inhibitor of EZH2, showed that EZH2 regulates genes involved in lipid homeostasis, and cysteine-methionine metabolism. Among the 13 EZH2 target genes identified by transcriptomic and epigenomic profiling, we selected BHMT and CDO1, which were significantly associated with poor survival in HCC patients. When HCC cells were treated with Tazemetostat, the expression levels of the BHMT and CDO1 genes increased, while the expression levels of ferroptosis marker genes, such as FSP1, NFS1, and SLC7A11, decreased. This suggests that inhibiting EZH2 may have potential therapeutic benefits in HCC by regulating the expression of genes involved in important biological processes. Our study suggests that EZH2 epigenetically regulates ferroptosis by controlling cysteine metabolism in HCC.
2024-10-25 | GSE237951 | GEO
Project description:Epigenetic dysregulation is closely associated with the pathogenesis of hepatocellular carcinoma (HCC). Enhancer of zeste homolog 2 (EZH2) is a key protein involved in the exacerbation of various cancers, including HCC. Despite several clinical trials of epigenetic therapies targeting EZH2, the mechanisms underlying EZH2-mediated gene suppression in HCC are not fully understood. In this study, we investigated EZH2-mediated transcriptional programs under EZH2-selective inhibition through an integrative analysis of epigenomic (ATAC-seq) and transcriptomic (RNA-seq) approaches. To determine the impact of EZH2 dysfunction, we measured the levels of H3K27me3 and EZH2 expression using flow cytometry and reverse transcription quantitative real-time PCR (RT-qPCR), respectively. Notably, we found that higher expression of EZH2 was significantly correlated with poorer survival among HCC patients by reanalyzing transcriptomes in the cancer genome atlas (TCGA). Inhibition of EZH2 with Tazemetostat (EPZ-6438), a selective inhibitor of EZH2, showed that EZH2 regulates genes involved in lipid homeostasis, and cysteine-methionine metabolism. Among the 13 EZH2 target genes identified by transcriptomic and epigenomic profiling, we selected BHMT and CDO1, which were significantly associated with poor survival in HCC patients. When HCC cells were treated with Tazemetostat, the expression levels of the BHMT and CDO1 genes increased, while the expression levels of ferroptosis marker genes, such as FSP1, NFS1, and SLC7A11, decreased. This suggests that inhibiting EZH2 may have potential therapeutic benefits in HCC by regulating the expression of genes involved in important biological processes. Our study suggests that EZH2 epigenetically regulates ferroptosis by controlling cysteine metabolism in HCC.
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Project description:The Polycomb group (PcG) protein enhancer of zeste homolog 2 (EZH2) plays an essential role in histone methylation-mediated epigenetic gene silencing. We demonstrate that under physiological conditions, cyclin-dependent kinase 1 (CDK1) and 2 (CDK2) bind to and phosphorylate EZH2 at threonine 350 (T350) in an evolutionally conserved motif. T350 phosphorylation is required for EZH2 function in silencing of genes that promote differentiation and inhibit proliferation and migration. Blockage of T350 phosphorylation by generating a T350A mutation largely diminishes the global effect of EZH2 on gene silencing. Seven experiments have been designed. LNCaP cells were transfected with si-Control, si-EZH2, si-EZH2 plus RNAi resistant EZH2 plasmid, or si-EZH2 plus RNAi resistant T350A mutated EZH2 plsamid for 60 hours, or treated with DMSO, 5 uM TSA, or 10 uM Roscovitine for 24 hours. Two replicates per experiment.
2010-11-02 | E-GEOD-20433 | biostudies-arrayexpress