Abstract
The cancer preventive properties of the essential nutrient selenium are partly mediated through selenoproteins. Herein, the effect of individual and combined down‐regulation of the 15 kDa selenoprotein (Sep15) and thioredoxin reductase 1 (TR1) in mouse colon carcinoma CT26 cells was examined. shRNA knockdown of either Sep15 or TR1 inhibited their anchorage‐dependent and ‐ independent cell growth, primary tumor growth and lung metastasis. Surprisingly, double knockdown of Sep15 and TR1 reversed the effects seen in single knockdowns. FACS analysis revealed that the significant G2/M cell cycle arrest in shSep15 cells was no longer observed in cells lacking both Sep15 and TR1. To investigate the molecular targets affected by single vs. double knockdown, gene expression was analyzed in control, Sep15‐, TR1‐ and Sep15/TR1‐knockdown CT26 cells using microarrays. Our analyses revealed that the expression of GBP‐1, the top upregulated gene in shSep15 cells, was not affected in shSep15/TR1 cells. The results suggest that the independent down‐regulation of either Sep15 or TR1, but not the double‐knockdown, resulted in changes of the cancer phenotype of mouse colon carcinoma cells. Funded by NCI Intramural support, the Cancer Prevention Fellowship Program, and NIH grants.
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