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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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE25884 | GEO | 2011/08/08

SECONDARY ACCESSION(S): PRJNA135817

REPOSITORIES: GEO

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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

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Project description:CRPC remains AR dependent. There are multiple mechanisms for reactivation of AR including expression of constitutively active AR splices variant AR-V7 (AR3). Earlier studies suggest that though the variants regulate many of the same genes as AR, they also have unique targets. Another argument is that the variant is a “weak” AR. We have used an LNCaP cell line that expresses AR-V7 in response to doxycycline to compare DNA interactions of the two isoforms and to identify differential regulation of target genes. ChIP-exo method was used to map AR and AR-V7 interaction with DNA in LNCaP engineered cell line (LNCaP AR-V7) at single base resolution.

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AR-V7 targets the oncogenic genes in castration resistant prostate cancer. [ChIP]

Project description:AR-V7 targets the oncogenic genes in castration resistant prostate cancer. [ChIP]

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identifying all AR binding regions in PC346C cell line

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Diverse AR-V7 cistromes in castration-resistant prostate cancer are governed by HoxB13

Project description:The constitutively active androgen receptor (AR) splice variant 7 (AR-V7) plays an important role in the progression of castration-resistant prostate cancer (CRPC). Although biomarker studies established the role of AR-V7 in resistance to AR-targeting therapies, how AR-V7 mediates genomic functions in CRPC remains largely unknown. Using a ChIP-exo approach, we show AR-V7 binds to distinct genomic regions and recognizes a full-length androgen-responsive element in CRPC cells and patient tissues. Remarkably, we find dramatic differences in AR-V7 cistromes across diverse CRPC cells and patient tissues, regulating different target gene sets involved in CRPC progression. Surprisingly, we discover that HoxB13 is universally required for and colocalizes with AR-V7 binding to open chromatin across CRPC genomes. HoxB13 pioneers AR-V7 binding through direct physical interaction, and collaborates with AR-V7 to up-regulate target oncogenes. Transcriptional coregulation by HoxB13 and AR-V7 was further supported by their coexpression in tumors and circulating tumor cells from CRPC patients. Importantly, HoxB13 silencing significantly decreases CRPC growth through inhibition of AR-V7 oncogenic function. These results identify HoxB13 as a pivotal upstream regulator of AR-V7-driven transcriptomes that are often cell context-dependent in CRPC, suggesting that HoxB13 may serve as a therapeutic target for AR-V7-driven prostate tumors.

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