Cancer: Breast cancer, prostate cancer

Action: Anti-metastastatic

Prostate Cancer

Sulforaphane is isolated from varieties of broccoli and other edible cruciferous vegetables as well as the root of Angelica sinensis (Oliv.) Diels (abbreviated as AS) (Danggui), which has a long history in Asian herbal medicine. A major constituent of Angelica sinensis, sulforaphane, is also found in cruciferous vegetables. It inhibits myostatin and increases cell viability in skeletal muscle satellite cells (Alway et al., 2002).

There is preclinical evidence that oral administration of D,L-sulforaphane (SFN) can decrease the incidence or burden of early-stage prostate cancer (PIN) and well-differentiated cancer (WDC), but not late-stage poorly differentiated cancer (PDC). SFN treatment caused in vivo autophagy as evidenced by transmission electron microscopy. Mechanistic studies showed that prevention of prostate cancer and metastasis by the SFN+CQ was associated with decreased cell proliferation, increased apoptosis, alterations in protein levels of autophagy regulators Atg5 and phospho-mTOR, and suppression of biochemical features of epithelial-mesenchymal transition. Plasma proteomics identified protein expression signature that may serve as biomarker of SFN+CQ exposure/response (Vyas et al., 2013a).

Exposure of PC-3 and DU145 human prostate cancer cells to D,L-Sulforaphane (SFN) resulted in induction of vimentin protein, which was accompanied by down-regulation of E-cadherin protein expression. The SFN-mediated induction of vimentin was also observed in a normal human prostate epithelial cell line. RNA interference of vimentin did not have any appreciable effect on early or late apoptosis resulting from SFN exposure.

On the other hand, SFN-mediated inhibition of PC-3 and DU145 cell migration was significantly augmented by knockdown of the vimentin protein. Knockdown of vimentin itself was inhibitory against cell migration. The SFN-treated cells also exhibited induction of PAI-1, which is an endogenous inhibitor of urokinase-type plasminogen activator system (Vyas & Singh, 2013b).

References

Alway SE, Degens H, Lowe DA, Krishnamurthy G. (2002). Increased myogenic repressor Id mRNA and protein levels in hindlimb muscles of aged rats. Am J Physiol Regul Integr Comp Physiol, 282(2):R411-22.

Totušek J, Tříska J, Lefnerová D, et al. (2011). Contents of Sulforaphane and Total Isothiocyanates, Antimutagenic Activity, and Inhibition of Clastogenicity in Pulp Juices from Cruciferous Plants. Czech J. Food Sci, 29(5): 548–556.

Vermeulen M, Klšpping-Ketelaars IW, van den Berg R, Vaes WH. (2008). Bioavailability and kinetics of sulforaphane in humans after consumption of cooked versus raw broccoli. J Agric Food Chem, 56(22):10505-9.

Vyas AR, Hahm E-R, Arlotti JA, et al. (2013a). Chemoprevention of Prostate Cancer by D,L-Sulforaphane Is Augmented by Pharmacological Inhibition of Autophagy. Cancer Research, 73(17). doi: 10.1158/0008-5472.CAN-13-0755

Vyas AR, Singh SV. (2013b). Functional relevance of D,L-sulforaphane-mediated induction of vimentin and plasminogen activator inhibitor-1 in human prostate cancer cells. Eur J Nutr..