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Elevated level of SUMOylated IRF-1 in tumor cells interferes with IRF-1-mediated apoptosis.

SUMOylation of transcription factors often attenuates transcription activity. This regulation of protein activity allows more diversity in the control of gene expression. Interferon regulatory factor-1 (IRF-1) was originally identified as a regulator of IFN-alpha/beta, and its expression is induced by viral infection or IFN stimulation. Accumulating evidence supports the theory that IRF-1 functions as a tumor suppressor and represses the transformed phenotype. Here we report that the level of SUMOylated IRF-1 is elevated in tumors. Site-directed mutagenesis experiments disclose that the SUMOylation sites of IRF-1 are identical to the major ubiquitination sites. Consequently, SUMOylated IRF-1 displays enhanced resistance to degradation. SUMOylation of IRF-1 attenuates its transcription activity, and SUMOylated IRF-1 inhibits apoptosis by repression of its transcriptional activity. These data support a mechanism whereby SUMOylation of IRF-1 inactivates its tumor suppressor function, which facilitates resistance to the immune response.

Pubmed ID: 17942705


  • Park J
  • Kim K
  • Lee EJ
  • Seo YJ
  • Lim SN
  • Park K
  • Rho SB
  • Lee SH
  • Lee JH


Proceedings of the National Academy of Sciences of the United States of America

Publication Data

October 23, 2007

Associated Grants


Mesh Terms

  • Apoptosis
  • Cell Line, Tumor
  • Humans
  • Interferon Regulatory Factor-1
  • Neoplasms
  • Protein Processing, Post-Translational
  • Small Ubiquitin-Related Modifier Proteins
  • Thermodynamics
  • Transcription, Genetic