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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Delineation of AR oncogenic functions in hepatocellular carcinoma

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

SUBMITTER: Hai Feng

PROVIDER: E-GEOD-25884 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Cell cycle-related kinase is a direct androgen receptor-regulated gene that drives β-catenin/T cell factor-dependent hepatocarcinogenesis.

Feng Hai H Cheng Alfred S L AS Tsang Daisy P DP Li May S MS Go Minnie Y MY Cheung Yue S YS Zhao Gui-jun GJ Ng Samuel S SS Lin Marie C MC Yu Jun J Lai Paul B PB To Ka F KF Sung Joseph J Y JJ

The Journal of clinical investigation 20110711 8

Hepatocellular carcinoma (HCC) is the fifth most common cancer worldwide. It is more prevalent in men than women. Related to this, recent genetic studies have revealed a causal role for androgen receptor (AR) in hepatocarcinogenesis, but the underlying molecular mechanism remains unclear. Here, we used genome-wide location and functional analyses to identify a critical mediator of AR signaling - cell cycle-related kinase (CCRK) - that drives hepatocarcinogenesis via a signaling pathway dependent ...[more]

PMID: 21747169

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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. 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.

2011-05-31 | E-GEOD-17733 | biostudies-arrayexpress

Delineation of AR oncogenic functions in hepatocellular carcinoma

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Homo sapiens

Project description:PLC/PRF/5 cells ChIP on CHIP

| PRJNA393569 | ENA

PLC/PRF/5 cells ChIP on CHIP

Project description:PLC/PRF/5 cells were harvested for chromatin immunoprecipitation followed by CHIP analysis performed on Aligent platform.

2017-07-10 | GSE100968 | 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

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