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. 2015 Dec 12;16(12):29732–29743. doi: 10.3390/ijms161226195

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© 2015 by the authors; licensee MDPI, Basel, Switzerland.

This article is an open access article distributed under the terms and conditions of the Creative Commons by Attribution (CC-BY) license (http://creativecommons.org/licenses/by/4.0/).

PMC Copyright notice

Schematic presentation of proposed molecular epigenetic mechanism of sulforaphane’s action including interdependence between histone modification and DNA methylation. SFN, sulforaphane; HDACs, histone deacetylases; RARβ2, nuclear retinoic acid receptor β2; AP-1, activator protein 1 (transcription factor); p21, cyclin-dependent kinase inhibitor 1; PCNA, proliferating cell nuclear antigen; DNMT1, DNA (cytosine-5-)-methyltransferase 1; PTEN, phosphate and TENsin homologue; MAPK Signaling Pathway (also known as the Ras-Raf-MEK-ERK pathway), the extracellular signal-regulated kinase pathway;—She, adaptor protein; Ras, GTPase (cellular signal transduction); Raf, kinase (activates MAP2K, which activates MAPK); MAPK, mitogen-activated protein kinase; Cyclin D2, member of the family of D-type cyclins; ERα, estrogen receptor alpha; hTERT human telomerase reverse transcriptase.