Androgen receptor-driven chromatin looping in prostate cancer

Dayong Wu, Chunpeng Zhang, Yanping Shen, Kenneth P. Nephew, Qianben Wang

Research output: Contribution to journalReview article

34 Citations (Scopus)

Abstract

The androgen receptor (AR) is important for prostate cancer development and progression. Genome-wide mapping of AR binding sites in prostate cancer has found that the majority of AR binding sites are located within non-promoter regions. These distal AR binding regions regulate AR target genes (e.g. UBE2C) involved in prostate cancer growth through chromatin looping. In addition to long-distance gene regulation, looping has been shown to induce spatial proximity of two genes otherwise located far away along the genomic sequence and the formation of double-strand DNA breaks, resulting in aberrant gene fusions (e.g. TMPRSS2-ERG) that also contribute to prostate tumorigenesis. Elucidating the mechanisms of AR-driven chromatin looping will increase our understanding of prostate carcinogenesis and may lead to the identification of new therapeutic targets.

Original languageEnglish (US)
Pages (from-to)474-480
Number of pages7
JournalTrends in Endocrinology and Metabolism
Volume22
Issue number12
DOIs
StatePublished - Dec 1 2011

Fingerprint

Androgen Receptors
Chromatin
Prostatic Neoplasms
Prostate
Carcinogenesis
Binding Sites
Genes
Double-Stranded DNA Breaks
Chromosome Mapping
Gene Fusion
Growth

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology

Cite this

Androgen receptor-driven chromatin looping in prostate cancer. / Wu, Dayong; Zhang, Chunpeng; Shen, Yanping; Nephew, Kenneth P.; Wang, Qianben.

In: Trends in Endocrinology and Metabolism, Vol. 22, No. 12, 01.12.2011, p. 474-480.

Research output: Contribution to journalReview article

Wu, Dayong ; Zhang, Chunpeng ; Shen, Yanping ; Nephew, Kenneth P. ; Wang, Qianben. / Androgen receptor-driven chromatin looping in prostate cancer. In: Trends in Endocrinology and Metabolism. 2011 ; Vol. 22, No. 12. pp. 474-480.
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