Histone Modifications and Chromatin Organization in Prostate Cancer

Abstract

Epigenetic mechanisms, including histone modifications, nucleosomal remodeling and chromosomal looping, contribute to the onset and progression of prostate cancer. Recent technical advances significantly increase our understanding of the genome-wide epigenetic regulation of gene expression in prostate cancer. Aberrant genomic distribution and global level of histone modifications, nucleosome repositioning at the gene promoter and enhancer regions, as well as androgen receptor-mediated chromosomal looping may lead to the silencing of tumor suppressor genes and the activation of proto-oncogenes. In addition, androgen receptor-induced chromosomal looping facilitates recurrent gene fusion in prostate cancer. Studies in epigenetic regulation have translational implications in the identification of new biomarkers and the development of new therapies in prostate cancer.

KEYWORDS::

• bioinformatics
• CHIA-PET
• ChIP-seq
• chromatin organization
• epigenome
• Hi-C
• histone modification
• next-generation sequencing
• prostate cancer

Acknowledgements

The authors also thank Drs Nancy Weigel and Tim Huang for critical reviewing of the manuscript, and Anna Rorick for editorial assistance.

Financial & competing interests disclosure

This work was supported by the National Cancer Institute Awards R00 CA126160, U54 CA 113001, and The Ohio State University Comprehensive Cancer Center (to Qianben Wang); the Department of Defense (PC094421) and the 973 project (2010CB944900) of China (to Wei Li). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

Additional information

Funding

This work was supported by the National Cancer Institute Awards R00 CA126160, U54 CA 113001, and The Ohio State University Comprehensive Cancer Center (to Qianben Wang); the Department of Defense (PC094421) and the 973 project (2010CB944900) of China (to Wei Li). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed. No writing assistance was utilized in the production of this manuscript.