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ARS Home » Plains Area » Grand Forks, North Dakota » Grand Forks Human Nutrition Research Center » Dietary Prevention of Obesity-related Disease Research » Research » Publications at this Location » Publication #247876
Title: Prolonged Sulforaphane Treatment Activates Extracellular-Regulated Kinase 1/2 Signaling in Nontumorigenic Colon Cells but not Colon Cancer Cells

Author
item Zeng, Huawei
item TRUJILLO, OLIVIA - University Of Arizona
item MOYER, MARY - Incell Corporation
item Botnen, James

Submitted to: Journal of Federation of American Societies for Experimental Biology
Publication Type: Abstract Only
Publication Acceptance Date: 12/15/2009
Publication Date: 4/24/2010
Citation: Zeng, H., Trujillo, O., Moyer, M.P., Botnen, J.H. 2010. Prolonged Sulforaphane Treatment Activates Extracellular-Regulated Kinase 1/2 Signaling in Nontumorigenic Colon Cells but not Colon Cancer Cells. Journal of Federation of American Societies for Experimental Biology. 24:928.4.

Interpretive Summary:

Technical Abstract: Sulforaphane (SFN) is a naturally occurring member of the isothiocyanate family of chemopreventive agents and the induction of cell cycle arrest and apoptosis is a key mechanism by which SFN exerts its colon cancer prevention. However, little is known about the differential effects of SFN on colon cancer and normal cells. In this study, we demonstrated that prolonged SFN (5, 10 or 15 'mol/L) exposure (72 h) inhibited cell proliferation up to 95% in colon cancer cells (HCT116) and 52% in normal colon mucosa-derived (NCM460) cells, respectively. Our data also showed that prolonged SFN exposure led to the significant induction of apoptosis and G2/M cell cycle arrest in HCT116, but to much less extent in NCM460 cells. Furthermore, the examination of mitogen-activated protein kinase (MAPK) signaling status revealed that prolonged SFN treatment strongly up-regulated the extracellular-regulated kinase ½ (ERK1/2) in NCM460 but not HCT116 cells. Taken together, the activation of ERK1/2 in NCM460 but not HCT116 cells may play a critical role in SFN’s stronger potential of inhibiting colon cancer cell proliferation when compared with normal colon cells.