Genomics

Dataset Information

25

Genome-wide location map of Polycomb in prostate cancer


ABSTRACT: We used chromatin immunoprecipitation (ChIP) in combination with human promoter microarrays to idnetify SUZ12 and H3K27me3-occupied gene promoters in prostate cancer cells and tissues. We observed a common set of SUZ12 and H3K27me3-occupied genes in LNCaP cells, and metastatic prostate cancer tissues across individuals as well as tissue types of the metastatic sites. We also found significant overlap of cancer polycomb targets with previously published embryonic stem cell polycomb targets. In addition, a strong association between cancer polycomb targets with prostate cancer outcome was observed. We developed a cancer Polycomb Repression Signature, comprised direct targets of PRC2 silencing in cancer, that is predictive of cancer outcome in multiple expression profling datasets of tumors. Keywords: protein-DNA interaction Overall design: SUZ12 and H3K27me3 occupancy were tested in LNCaP cells as well as 3 metastatic prostate cancer tissues from independent patients. Using the proximal promoter arrays, we are assaying binding in -1.0kb to 0.3kb promoter regions of over 17,000 human genes. We first tested the co-ocupancy of SUZ12 and H3K27me3 in LNCaP prostate cancer cell lines, then extended to 2 metastatic prostate cancer tissue (to the liver). We lastly examined H3K27me3 occupancy in another metastatic prostate cancer tissue from different metasatic site (to the lung) of an independent patient.

INSTRUMENT(S): Agilent-013902 Human Proximal Promoter ChIP-on-Chip Set, Microarray 1 of 2 G4481A

SUBMITTER: Jindan Yu  

PROVIDER: GSE9069 | GEO | 2007-11-01

SECONDARY ACCESSION(S): PRJNA102581

REPOSITORIES: GEO

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Publications


The Polycomb Group (PcG) protein EZH2 is a critical component of a multiprotein complex that methylates Lys(27) of histone 3 (H3K27), which consequently leads to the repression of target gene expression. We have previously reported that EZH2 is overexpressed in metastatic prostate cancer and is a marker of aggressive diseases in clinically localized solid tumors. However, the global set of genes directly regulated by PcG in tumors is largely unknown, and thus how PcG mediates tumor progression r  ...[more]

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