Histone H2A.Z deregulation in prostate cancer. Cause or effect?

Genetic and epigenetic changes are at the root of all cancers. The epigenetic component involves alterations of the post-synthetic modifications of DNA (methylation) and histones (histone posttranslational modifications, PTMs) as well as of those of their molecular writers, readers, and erasers. Noncoding RNAs (ncRNA) can also play a role. Here, we focus on the involvement of histone alterations in cancer, in particular that of the histone variant H2A.Z in the etiology of prostate cancer. The structural mechanisms putatively responsible for the contribution of H2A.Z to oncogenic gene expression programs are first described, followed by what is currently known about the involvement of this histone variant in the regulation of androgen receptor regulated gene expression. The implications of this and their relevance to oncogene deregulation in different stages of prostate cancer, including the progression toward androgen independence, are discussed. This review underscores the increasing awareness of the epigenetic contribution of histone variants to oncogenic progression.