Prostate cancer is the second most common cancer in men worldwide and the second leading cause of cancer related mortality. The major identified risk factors for development of prostate cancer include age, family history and race. Current treatment regimens lead to mixed results due to many varying risk factors and side effects. This complication in addition to the high rate of over diagnosis with prostate specific antigen (PSA) screening necessitate the need for primary chemoprevention1. Studies have shown that consumption of cruciferous vegetables lowers the risk of prostate cancer. Sulforaphane (SFN) is an isothiocyanate that can be found in cruciferous vegetables such as broccoli, Brussels sprouts and cabbage. It is produced by the hydrolysis of glucoraphanin by myrosinase2. SFN has been known to have chemopreventative properties including the activation of phase II enzymes as measured by quinone reductase activity and inhibition of histone deacetylase (HDAC) evidenced by the increased activity of b-catenin responsive reporter2,3. However, recent studies suggest that SFN holds many other chemopreventive properties. Based on RNA sequencing, SFN was shown to decrease the expression of Sp1 transcription factors which caused a decrease in prostate cancer cell proliferation4. Western blot analysis also showed decreased expression of the chemokine receptor CXCR4 in prostate cancer cells after treatment with SFN5. Using methyl-DNA immunoprecipitation and genome wide DNA methylation array SFN treatment was shown to decrease DNA methyltransferase expression in normal prostate epithelial cells and androgen independent/dependent prostate cancer cells6. Currently, 5a reductase inhibitors are the only class of drugs that have been shown to reduce incidence of prostate cancer in large randomized trials. However, their efficacy as a chemopreventive agent remains uncertain due to high cost and risk of developing high grade prostate cancer7. SFNs low toxicity and multiple mechanisms makes it an attractive potential chemopreventative agent. Further research in clinical settings is needed harness and understand the potential of SFN as a viable chemopreventative agent.
- Attard, C. Parker, R.A. Eeles, F. Schröder, S.A. Tomlins, I. Tannock, C.G. Drake, J.S. De Bono. Prostate cancer. Lancet. 2016;387:70–82
- Myzak MC, Karplus PA, Chung FL, Dashwood RH. A novel mechanism of chemoprotection by sulforaphane: inhibition of histone deacetylase. Cancer Res. 2004; 64:5767–74.
- Brooks JD, Paton VG, Vidanes G. Potent induction of phase 2 enzymes in human prostate cells by sulforaphane. Cancer Epidemiol Biomarkers Prev. 2001;10:949–54.
- Beaver LM, Buchanan A, Sokolowski EI, et al. Transcriptome analysis reveals a dynamic and differential transcriptional response to sulforaphane in normal and prostate cancer cells and suggests a role for Sp1 in chemoprevention. Molecular nutrition & food research. 2014;58(10):2001-2013.
- Sakao K, Vyas AR, Chinni SR, Amjad AI, Parikh R, Singh SV. CXCR4 is a novel target of cancer chemopreventive isothiocyanates in prostate cancer cells. Cancer Prev Res (Phila) 2015;8:365–374.
- Wong CP, Hsu A, Buchanan A, et al. Effects of Sulforaphane and 3,3′-Diindolylmethane on Genome-Wide Promoter Methylation in Normal Prostate Epithelial Cells and Prostate Cancer Cells. Futscher BW, ed. PLoS ONE. 2014;9(1):e86787.
- Amjad AI, Parikh RA, Appleman LJ, Hahm E-R, Singh K, Singh SV. Broccoli-Derived Sulforaphane and Chemoprevention of Prostate Cancer: From Bench to Bedside. Current pharmacology reports. 2015;1(6):382-390.