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Comment
. 2010 May 18;17(5):415-6.
doi: 10.1016/j.ccr.2010.04.022.

Coordinate transcriptional regulation by ERG and androgen receptor in fusion-positive prostate cancers

Yu Chen  1 , Charles L Sawyers
Affiliations
Comment

Coordinate transcriptional regulation by ERG and androgen receptor in fusion-positive prostate cancers

Yu Chen et al. Cancer Cell. .

Abstract

In this issue of Cancer Cell, Yu and colleagues mapped the genomic binding sites of ERG and androgen receptor, two crucial transcription factors in prostate cancer. There is an extraordinary degree of overlap between binding sites, with the suggestion that ERG inhibits androgen receptor-mediated differentiation and promotes EZH2-mediated dedifferentiation.

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Figures

Figure 1
Figure 1. Coordinate regulation of target genes by androgen receptor and ERG
AR binding at enhancers of AR target gene causes looping and gene activation. The “GGAA” ETS motif is highly enriched at AR binding sites raising the possibility that an unidentified ETS protein (not ERG) may coordinately regulate transcription in normal prostate cells (top). In ERG+ prostate cancer, ERG now localizes at these sites, perhaps displacing an “endogenous” ETS factor, as well as gene promoters and inhibits AR mediates transcriptional activation.
See this image and copyright information in PMC

Comment on

References

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