DNA Methylation as a Dynamic Regulator of Development and Disease Processes: Spotlight on the Prostate

Abstract

Prostate development, benign hyperplasia and cancer involve androgen and growth factor signaling as well as stromal–epithelial interactions. We review how DNA methylation influences these and related processes in other organ systems such as how proliferation is restricted to specific cell populations during defined temporal windows, how androgens elicit their actions and how cells establish, maintain and remodel DNA methylation in a time and cell specific fashion. We also discuss mechanisms by which hormones and endocrine disrupting chemicals reprogram DNA methylation in the prostate and elsewhere and examine evidence for a reawakening of developmental epigenetic pathways as drivers of prostate cancer and benign prostate hyperplasia.

Genetics and genomics etiology of nonsyndromic orofacial clefts

“…Beyond variations in DNA, the epigenome is increasingly being reported as relevant to the etiology of diseases. This has been well established in cancer, obesity, and diabetes (Keil and Vezina ; Wahlqvist et al. ).…”

“…Beyond variations in DNA, the epigenome is increasingly being reported as relevant to the etiology of diseases. This has been well established in cancer, obesity, and diabetes (Keil and Vezina 2015;Wahlqvist et al 2015). The impacts of variations in DNA methylation and acetylation, otherwise known as epi-mutations, have been reported to last beyond three generations (El Hajj et al 2014).…”

The interplay between the lysine demethylase KDM1A and DNA methyltransferases in cancer cells is cell cycle dependent

“…Aberrant DNA methylation is a well-characterized epigenetic hallmark of several cancers [ 1 , 54 – 56 ]. Dysregulated expression of DNMT genes has been reported for various human tumors [ 57 ].…”

Human trophoblasts are primarily distinguished from somatic cells by differences in the pattern rather than the degree of global CpG methylation

“…Global methylation changes are associated with developmental stages and pathological conditions and can influence cell differentiation (Jackson et al, 2004; Keil and Vezina, 2015). In the placenta, global hypomethylation has been hypothesised to fulfil a uniquely conserved functional role, regulating the gene expression necessary for adequate placental development (Bianco-Miotto et al, 2016; Schroeder et al, 2015).…”