Sulforaphane

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Background

Sulforaphane is an inducer of chemopreventative enzymes via Keap1-Nrf2 signaling [1]. Sulforaphane is present naturally in widely consumed vegetables and has a particularly high concentration in broc-coli [1].
The Keap1-Nrf2 pathway is the major regulator of cytoprotective responses to oxidative and electrophilic stress. Nrf2 triggers the signaling pathways to prevent cancer initiation and progression in normal and premalignant tissues. In fully malignant cells, Nrf2 activity provides growth advantage by increasing cancer chemoresistance and enhancing tumor cell growth [2].
In human colon carcinoma cells (HT29) cells, sulforaphane at 15 μM inhibited cell growth and induced cell death. Sulforaphane induced a cell cycle arrest in a dose-dependent manner, followed by cell death. Sulforaphane induced cell cycle arrested in G2 -M Phase, which was correlated with increased expression of cyclins A and B1. Sulforaphane increased expression of the proapoptotic protein bax, the release of cytochrome c from the mitochondria to the cytosol, and the proteolytic cleavage of poly(ADP-ribose) polymerase [1].

[1] Gamet-Payrastre L, Li P, Lumeau S, et al. Sulforaphane, a naturally occurring isothiocyanate, induces cell cycle arrest and apoptosis in HT29 human colon cancer cells[J]. Cancer research, 2000, 60(5): 1426-1433.
[2] Kansanen E, Kuosmanen S M, Leinonen H, et al. The Keap1-Nrf2 pathway: mechanisms of activation and dysregulation in cancer[J]. Redox biology, 2013, 1(1): 45-49.