Active vitamin D induces gene-specific hypomethylation in prostate cancer cells developing vitamin D resistance.

Prostate cancer (PCa) is a leading cause of cancer death in men. Despite the antiproliferative effects of 1α,25-dihydroxyvitamin D [1,25(OH)D] on PCa, accumulating evidence indicates that 1,25(OH)D promotes cancer progression by increasing genome plasticity. Our investigation of epigenetic changes associated with vitamin D insensitivity found that 1,25(OH)D treatment reduced the expression levels and activities of DNA methyltransferases 1 and 3B (DNMT1 and DNMT3B, respectively).