Vitamin D has wide regulatory effects on histone demethylase genes

KDM5B histone demethylase controls epithelial-mesenchymal transition of cancer cells by regulating the expression of the microRNA-200 family

“…33,38 Increased EZH2 activity in cancer was shown to cause repression of numerous microRNAs, including miR-200b and miR-200c, through H3K27me3 regulation at these loci. 39 A recent paper also demonstrated that knockdown of JMJD3 H3K27 demethylase decreased the expression of miR-200b and miR-200c for upregulation of EMT inducers such as ZEB1 and ZEB2, 40 suggesting the importance of H3K27 methylation in the regulation of miR-200 family expression. Furthermore, a recent genome-wide profiling of histone methylation during EMT revealed strong correlations between the dynamic changes of histone methylations and gene expression.…”

Vitamin D, reactive oxygen species and calcium signalling in ageing and disease

“…For example, hypermethylation of promotors in GABAergic neurons may contribute to the phenotypic remodelling responsible for schizophrenia and bipolar disorder [30]. Vitamin D modulates methylation by inducing the expression of a number of key DNA demethylases such as Jumonji domain-containing protein 1A and 3 (JMJD1A, JMJD3) and lysine-specific demethylase 1 and 2 (LSD1, LSD2) that contributes to its ability to maintain phenotypic stability [31].…”

Epigenetic Impact of Bioactive Dietary Compounds in Cancer Chemoprevention

“…In the colon cancer SW480-ADH cells, calcitriol increased the expression of the HDM Jumonji JMJD3, which upregulated the epithelial-to-mesenchymal transition inducers SNAIL1 and ZEB1, while it downregulated the epithelial proteins, including E-cadherin (Pereira et al 2011). Novel data indicate that calcitriol exerts its regulatory role via Jumonji C (JmjC) and lysine-specific demethylase (LSD) families of the HDMs (Pereira et al 2012). In addition, JMJD3 knockdown decreases the expression of miR-200b and miR-200c, two microRNAs targeting ZEB1 RNA (Pereira et al 2012).…”

“…In vitro studies demonstrated that calcitriol [1 alpha,25 Dihydroxyvitamin D(3)], an active metabolite of vitamin D, synergized the pro-apoptotic effect of HDAC inhibitors sodium butyrate (NaB), a natural short-chain fatty acid, and trichostatin A (TSA), a synthetic HDAC inhibitor, in the prostate cancer cells LNCaP, PC-3, and DU-145 (Rashid et al 2001). Calcitriol inhibited the expression of several HDMs and induced the expression of others (Pereira et al 2011(Pereira et al , 2012. In the colon cancer SW480-ADH cells, calcitriol increased the expression of the HDM Jumonji JMJD3, which upregulated the epithelial-to-mesenchymal transition inducers SNAIL1 and ZEB1, while it downregulated the epithelial proteins, including E-cadherin (Pereira et al 2011).…”