Interferon-alpha (Intron A) upregulates urokinase-type plasminogen activator receptor gene expression

Abstract

The regulation of urokinase plasminogen activator receptor (uPAR) gene expression by interferon-alpha (IFN-α, or Intron A) and interferon-gamma (IFN-γ) was studied in a HCT116 colon cancer cell line. uPAR mRNA levels were increased in a dose- and time-dependent manner in cells stimulated with IFN-α or IFN-γ. uPAR protein levels reflected IFN-α and IFN-γ induction of uPAR mRNA production. Cycloheximide, a protein synthesis inhibitor, also induced uPAR mRNA accumulation either alone or in combination with IFN-α or IFN-γ, suggesting that the effect on uPAR mRNA levels activated by IFN-α or IFN-γ does not require de novo protein synthesis. Both sodium butyrate and amiloride inhibited the uPAR mRNA levels induced by IFN-α or IFN-γ. These results may provide useful information for the treatment of patients receiving IFN-α or IFN-γ.