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ETS factors reprogram the androgen receptor cistrome and prime prostate tumorigenesis in response to PTEN loss
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ETS factors reprogram the androgen receptor cistrome and prime prostate tumorigenesis in response to PTEN loss
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Journal Article
ETS factors reprogram the androgen receptor cistrome and prime prostate tumorigenesis in response to PTEN loss
2013
Overview
Studies on a new conditional mouse model reveal that
ETS
transcription factors, which are often mutated in prostate cancer, cause transformation by altering the androgen-receptor cistrome, priming the prostate epithelium to respond to upstream signals such as
PTEN
loss.
Studies of ETS-mediated prostate oncogenesis have been hampered by a lack of suitable experimental systems. Here we describe a new conditional mouse model that shows robust, homogenous ERG expression throughout the prostate. When combined with homozygous
Pten
loss, the mice developed accelerated, highly penetrant invasive prostate cancer. In mouse prostate tissue, ERG markedly increased androgen receptor (AR) binding. Robust ERG-mediated transcriptional changes, observed only in the setting of
Pten
loss, included the restoration of AR transcriptional output and upregulation of genes involved in cell death, migration, inflammation and angiogenesis. Similarly, ETS variant 1 (ETV1) positively regulated the AR cistrome and transcriptional output in
ETV1
-translocated,
PTEN
-deficient human prostate cancer cells. In two large clinical cohorts, expression of
ERG
and
ETV1
correlated with higher AR transcriptional output in
PTEN
-deficient prostate cancer specimens. We propose that
ETS
factors cause prostate-specific transformation by altering the AR cistrome, priming the prostate epithelium to respond to aberrant upstream signals such as
PTEN
loss.
Publisher
Nature Publishing Group US,Nature Publishing Group
Subject
/ Animals
/ Cell Transformation, Neoplastic - genetics
/ Cell Transformation, Neoplastic - pathology
/ Chromatin Immunoprecipitation
/ DNA-Binding Proteins - metabolism
/ Humans
/ Male
/ Mice
/ Oncogene Proteins - metabolism
/ Principal Component Analysis
/ Prostatic Neoplasms - genetics
/ Prostatic Neoplasms - pathology
/ Proto-Oncogene Proteins c-ets - metabolism
/ PTEN Phosphohydrolase - deficiency
/ PTEN Phosphohydrolase - metabolism
/ Receptors, Androgen - genetics
/ Receptors, Androgen - metabolism
/ Signal Transduction - genetics
/ Transcription Factors - metabolism
/ Transcriptional Regulator ERG
/ Tumors
