Epigenetic modifications in prostate cancer

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  • Masahiro Sugiura
    Departments of Department of Urology Chiba University Graduate School of Medicine Chiba Japan
  • Hiroaki Sato
    Departments of Department of Urology Chiba University Graduate School of Medicine Chiba Japan
  • Manato Kanesaka
    Departments of Department of Urology Chiba University Graduate School of Medicine Chiba Japan
  • Yusuke Imamura
    Departments of Department of Urology Chiba University Graduate School of Medicine Chiba Japan
  • Shinichi Sakamoto
    Departments of Department of Urology Chiba University Graduate School of Medicine Chiba Japan
  • Tomohiko Ichikawa
    Departments of Department of Urology Chiba University Graduate School of Medicine Chiba Japan
  • Atsushi Kaneda
    Department of Molecular Oncology Chiba University Graduate School of Medicine Chiba Japan

Description

<jats:title>Abstract</jats:title><jats:p>Prostate cancer is a major cause of cancer‐related deaths among men worldwide. In addition to genomic alterations, epigenetic alterations accumulated in prostate cancer have been elucidated. While aberrant deoxyribonucleic acid hypermethylation in promoter CpG islands inactivates crucial genes associated with deoxyribonucleic acid repair, cell cycle, apoptosis or cell adhesion, aberrant deoxyribonucleic acid hypomethylation can lead to oncogene activation. Acetylation of histone is also deregulated in prostate cancer, which could cause aberrant super‐enhancer formation and activation of genes associated with cancer development. Deregulations of histone methylation, such as an increase of trimethylation at position 27 of histone H3 by enhancer of zeste homolog2 overexpression, or other modifications, such as phosphorylation and ubiquitination, are also involved in prostate cancer development, and inhibitors targeting these epigenomic aberrations might be novel therapeutic strategies. In this review, we provide an overview of epigenetic alterations in the development and progression of prostate cancer, focusing on deoxyribonucleic acid methylation and histone modifications.</jats:p>

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