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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 #187192


item Zeng, Huawei
item Briske Anderson, Mary
item Idso, Joseph
item Hunt, Curtiss

Submitted to: Federation of American Societies for Experimental Biology Conference
Publication Type: Abstract Only
Publication Acceptance Date: 11/10/2005
Publication Date: 3/7/2006
Citation: Zeng, H., Briske Anderson, M.J., Idso, J.P., Hunt, C. 2006. Selenium metabolite methylselenol inhibits migration and invasion potential of HT1080 tumor cells [abstract]. FASEB J. 20(5):A1011.

Interpretive Summary:

Technical Abstract: The anti-carcinogenic effects of selenium in nutrition are well established. Methylselenol has been hypothesized as a critical selenium metabolite for anticancer activity in vivo. To determine whether tumor cell migration, invasion, and the cell cycle characteristics are inhibited by methylselenol, we exposed HT1080 cells to methylselenol. Methylselenol, generated with seleno-L-methionine, is a substrate for methioninase. Submicromolar methylselenol exposure led to an increase in the G1 and G2 fractions with a concomitant drop in the S phase, indicating slower cell growth. Furthermore, methylselenol inhibited the migration and invasion rate of the tumor cells by up to 53% and 76%, respectively, when compared with the control tumor cells. Although all cells had increased matrix metalloproteinase (MMP) enzymatic activities of pro MMP 2 and pro MMP 9, the active form of MMP 2 was decreased in HT1080 cells cultured with methylselenol. In addition, methylselenol increased the protein levels of anti-metastasic tissue inhibitor metalloproteinase 1 (TIMP 1) and metalloproteinase-2 (TIMP 2). Collectively, these results demonstrate that submicromolar concentrations of methylselenol increase both pro-metastasis MMP 2 and 9 and anti metastasis TIMP 1, 2 expression. The apparent net effect of these changes is the inhibition of carcinogenic potential/activity.