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The Phytochemical Sulforaphane Appears to Prevent Cancer through Two Distinct Epigenetic Mechanisms

Genetic abnormalities are considered the primary cause of cancer, but epigenetic mechanisms, altering gene expression without affecting DNA sequence, are recognized as being of significant importance as well. Sulforaphane, a dietary compound abundantly produced in broccoli, cauliflower and other cruciferous vegetables, is known to possess anti-proliferative and pro-apoptotic activities in many cancer cells. Sulforaphane is known to inhibit histone deacetylases (HDACs), which can interfere with the normal function of tumor suppressor genes. Dr. Emily Ho and colleagues at Oregon State University have now identified DNA methylation as a second cancer-producing epigenetic mechanism regulated by sulforaphane (Hsu et al. Clinical Epigenetics 2011, 3:3). Cell cycle progression is regulated by cyclin-dependent kinases (CDKs) and their activities are further controlled by cyclins and CDK inhibitors. The investigators demonstrated that sulforaphane reduces DNA methlyation of the cyclin D2 promoter in prostate cancer cells, increasing cyclin D2 transcript levels. Epigenetic silencing through promoter hypermethylation and histone deacetylation is responsible for transcriptional repression of numerous tumor suppressor and growth regulatory genes in cancer cells. Sulforaphane may serve as a useful chemopreventative agent through regulating gene expression levels in cancers.

In addition to natural products such as sulforaphane, Enzo Life Sciences offers a comprehensive portfolio of kits and reagents relevant to epigenetics, including antibodies for the detection of key epigenetic-regulating enzymes and substrates, like modification-specific antibodies for methylated, phosphorylated, or acetylated epitopes.

 

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