Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

51 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Delineation of EZH2 oncogenic functions in hepatocellular carcinoma

ABSTRACT: The goal of this study was to delineate the important EZH2 direct target genes that mediate the oncogenic properties of EZH2 in HCC. The EZH2 direct target genes in two HCC cell lines were identified by chromatin immunoprecipitation microarray (ChIP-chip) analysis and later confirmed by independent ChIP-PCR. The functions of the target genes were further examined. Two human HCC cell lines, Huh7 and PLC/PRF/5 (PLC5), were grown in DMEM supplemented with 10% fetal bovine serum. ChIP assays were performed using anti-EZH2 antibody. The immunoprecipitated and input DNA were used to probe the Agilent human ChIP-chip arrays.

ORGANISM(S): Homo sapiens

SUBMITTER: Richard CHOY

PROVIDER: E-GEOD-17733 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

EZH2-mediated concordant repression of Wnt antagonists promotes β-catenin-dependent hepatocarcinogenesis.

Cheng Alfred S L AS Lau Suki S SS Chen Yangchao Y Kondo Yutaka Y Li May S MS Feng Hai H Ching Arthur K AK Cheung Kin F KF Wong Hoi K HK Tong Joanna H JH Jin Hongchuan H Choy Kwong W KW Yu Jun J To Ka F KF Wong Nathalie N Huang Tim H-M TH Sung Joseph J Y JJ

Cancer research 20110421 11

Enhancer of zeste homolog 2 (EZH2) is the catalytic subunit of the Polycomb-repressive complex 2 (PRC2) that represses gene transcription through histone H3 lysine 27 trimethylation (H3K27me3). Although EZH2 is abundantly present in various cancers, the molecular consequences leading to oncogenesis remain unclear. Here, we show that EZH2 concordantly silences the Wnt pathway antagonists operating at several subcellular compartments, which in turn activate Wnt/β-catenin signaling in hepatocellula ...[more]

PMID: 21512140

Similar Datasets

Delineation of AR oncogenic functions in hepatocellular carcinoma

Project description:The goal of this study was to delineate the important AR direct target genes that mediate the oncogenic properties of AR in HCC. The AR direct target genes in two HCC cell lines were identified by chromatin immunoprecipitation microarray (ChIP-chip) analysis and later confirmed by independent ChIP-PCR. The functions of the target genes were further examined. Two human HCC cell lines, Huh7 and PLC/PRF/5 (PLC5), were grown in DMEM supplemented with 10% fetal bovine serum. ChIP assays were performed using anti-AR antibody. The immunoprecipitated and input DNA were used to probe the Agilent human ChIP-chip arrays.

2011-08-07 | E-GEOD-25884 | biostudies-arrayexpress

Delineation of EZH2 oncogenic functions in hepatocellular carcinoma

Project description:The goal of this study was to delineate the important EZH2 direct target genes that mediate the oncogenic properties of EZH2 in HCC. The EZH2 direct target genes in two HCC cell lines were identified by chromatin immunoprecipitation microarray (ChIP-chip) analysis and later confirmed by independent ChIP-PCR. The functions of the target genes were further examined.

2011-05-31 | GSE17733 | GEO

Delineation of AR oncogenic functions in hepatocellular carcinoma

2011-08-08 | GSE25884 | GEO

Spreading of X-chromosome inactivation via a hierarchy of defined Polycomb stations

Project description:Binding of Polycomb repressive complex 2 (PRC2) and chromatin composition of the inactive X (Xi) before, during and after X chromosome inactivation reveal that spreading is driven by a combination of Xi-specific strong and moderate Ezh2 sites. Sequence context of these sites shows a moderate enrichment of SINEs and simple repeats. The general pattern of Ezh2 and H3K27me3 distribution over the chromosome reflect a graded concentration originating from strong Ezh2 sites, around which moderate sites are clustered, suggesting a hierarchy of Ezh2 sites govern spreading. ChIP-seq of Ezh2 and H3K27me3 as well as the three active marks H3K4me3, H3K36me3 and RNA-POLII-serine5 phosphorylation (RNA-polII-S5P) in female cell lines: undifferentiated embryonic stem (ES) cells (d0), differentiating ES cells (d7) and a transformed embryonic fibroblast cell line (MEF).

2012-11-01 | E-GEOD-36905 | biostudies-arrayexpress

Chip-chip from HepG2 cells with EZH2, SUZ12 and H3K27me3

Project description:Polycomb group (PcG) proteins including EZH2, SUZ12 and so on, which specifically catalyze trimethylation of histone 3 lysine 27 (H3K27me3), and methylated H3K27 can be recognized by other specific binding proteins to compress chromatin structure, leading to the transcriptional repression of the target genes. To completely understand the epigenetic profile and molecular network of PcG in HCC, we performed ChIP-on-chip screens with EZH2, SUZ12 and H3K27me3 antibodies in HepG2 cells. Comparison of ChIP-on-chip results from EZH2, SUZ12 and H3K27me3.

2013-11-13 | E-GEOD-52300 | biostudies-arrayexpress

LncRNA regulated by hnRNPAB in HCC cell lines

Project description:To reveal the HNRNPAB-regulated lncRNAs, we performed microarray analyses to screen differential lncRNAs in HCC cells after stable overexpression or knockdown of HNRNPAB. MHCC97H and HCCLM3 (HCC cell lines with high-metastatic potentials), PLC/PRF/5 and HepG2 (HCC cell lines with low-metastatic potentials) were used in this study. HepG2-control, HepG2-hnRNPAB, PLC/PRF/5-control, PLC/PRF/5-hnRNPAB, MHCC97H-control, MHCC97H-sh-hnRNPAB, HCCLM3-control, HCCLM3-sh-hnRNPAB were perpared with hU6-MCS-CBh-gcGFP-IRES-puromycin-shRNA-HNRNPAB/mock lentiviral and Ubi-MCS-SV40-EGFP-IRES-puromycin-HNRNPAB/mock cDNA lentiviral,respectively, each performed in triplicate.

2019-01-01 | GSE124516 | GEO

A cDNA microarray analysis was performed on shRNA KDs of EZH2, SUZ12, BMI1, or CBX8 HepG2 cells.

Project description:Polycomb group (PcG) proteins including EZH2, SUZ12 ,BMI1,CBX8 and so on, which specifically catalyze trimethylation of histone 3 lysine 27 (H3K27me3), and methylated H3K27 can be recognized by other specific binding proteins to compress chromatin structure, leading to the transcriptional repression of the target genes. To explore a potential functional implication of PcG components in HCC, we stably transfected HepG2 cells with either vectors or constructs expressing shRNA that specifically targets EZH2, SUZ12, BMI1, or CBX8. A cDNA microarray analysis was performed on shRNA KDs of EZH2, SUZ12, BMI1, or CBX8 HepG2 cells. To obtain a broader understanding of the molecular network of PcG in HCC, the whole genome microarray expression profiling was performed on shRNA KDs of EZH2, SUZ12, BMI1, or CBX8 HepG2 cells. Comparison of gene expression results from shRNA KDs of EZH2, SUZ12, BMI1 or CBX8 HepG2 cells.

2014-01-16 | E-GEOD-54108 | biostudies-arrayexpress

The RNA-seq of HCC specimens and the RIP-seq of HNRNPD in PLC cells and WT (DMSO or Compound C) and circLARP1B-Def (DMSO) PLC/PRF/5 cells

Project description:To investigate functional transcripts in metastatic HCC, we performed high-throughput RNA sequencing (RNA-seq) of tumors from 3 metastatic HCC and 3 non-metastatic HCC. And we performed RIP-seq human PLC/PRF/5 cells to investigate the HNRNPD binding transcripts. To investigate function of circLARP1B on AMPK pathway, we performed high-throughput RNA sequencing (RNA-seq) of WT (DMSO or Compound C) and circLARP1B-Def (DMSO) PLC/PRF/5 cells.

2023-04-02 | GSE217403 | GEO

Hepatic stellate cells mediates transcription of TNFSF14 in hepatocellular carcinoma cells via H2S/CSE-JNK/JunB signaling pathway

Project description:Purpose: Hepatic stellate cell (HSC) and Hydrogen sulfide (H2S) both play important roles in Hepatocellar carcinoma (HCC). Whereas, in the microenvironment of HCC, whether HSC participates in regulating the biological process of HCC cells by releasing H2S remains elusive. In this study, we investigate how activated HSC influence HCC fate. Methods: The effects of LX-2 and H2S on biological functions of HCC cells were analyzed with Flow cytometry and CCK-8. RNA-sequencing, Western blotting, Quantitative real-time reverse transcription PCR (RT-qPCR), siRNA, immunofluorescence and chromatin immunoprecipitation (ChIP) assays were carried out to examine the effect of H2S on JNK/JunB-TNFSF14 (tumor necrosis factor superfamily member 14) signaling pathway. Specimens from HCC patients were analyzed by using RT-qPCR and Western blotting assays for evaluating the expression of TNFSF14. Statistical analysis was used to analyze the correlation between TNFSF14 expression and clinical data of HCC patients. Results: LX-2 cells is able to induce HepG2 and PLC/PRF/5 cells apoptosis by releasing H2S. RNA- sequencing results showed that TNFSF14 gene was changed in both LX-2 and NaHS group. NaHS dosage and time-dependently up-regulated TNFSF14 mRNA and protein expression in both HepG2 and PLC/PRF/5 cells. NaHS treated in HCC cells led to JNK/JunB signaling pathway activating and greater binding of JunB to its responsive elements on TNFSF14 promoter. Impairment of TNFSF14 induction alleviated LX-2 and NaHS induced apoptosis of HepG2 and PLC/PRF/5 cells. Furthermore, mRNA and protein expressions of TNFSF14 in HCC tissues was lower than in the adjacent tissue. HCC patients with low expression of TNFSF14 have higher malignant degree and poor prognosis. Conclusions: Demonstration of the involvement of HSC-derived H2S in JNK/JunB mediated expression of TNFSF14 gene strongly indicates H2S palys an important role in the regulation of HCC apoptosis.

2022-03-22 | GSE193660 | GEO

Transcription profiling of by array of human hepatocellular carcinoma cells with RNAi knockdown of Wilm's Tumor 1 gene expression

Project description:The Wilms' tumor 1 gene (WT1) encodes a transcription factor involved in cell growth and development. As we previously reported WT1 expression is hardly detectable in normal hepatic tissue but is induced in liver cirrhosis. Although WT1 has been found to be overexpressed in a number of malignancies, the role of WT1 in hepatocarcinogenesis has not been clarified. We found that WT1 is expressed in several human hepatocellular carcinoma (HCC) cell lines including PLC/PRF/5 and HepG2, and in HCC tumor tissue in 42% of patients. WT1 small interfering RNAs did not affect proliferation rate of HCC cells but abrogated their resistance to anoikis. Transcriptome analysis of PLC/PRF/5 cells after WT1 knockdown demonstrated upregulation of 251 genes and downregulation of 321. Ninety per cent of the former corresponded to metabolic genes mostly those characterizing the mature hepatocyte phenotype. On the contrary, genes that decreased upon WT1 inhibition were mainly related to defense against apoptosis, cell cycle and tumor progression. In agreement with these findings WT1 expression increased the resistance of liver tumor cells to doxorubicin, a compound used to treat HCC. Interestingly, doxorubicin strongly enhanced WT1 expression in both HCC cells and normal human hepatocytes. Among different chemotherapeutics, induction of WT1 transcription was restricted to topoisomerase 2 inhibitors. When WT1 expression was prohibited doxorubicin caused a marked increase in caspase-3 activation. In conclusion, WT1 is expressed in a substantial proportion of HCC contributing to tumor progression and resistance to chemotherapy, suggesting that WT1 may be an important target for HCC treatment.

2008-10-26 | E-GEOD-12886 | 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