RASSF1A suppresses the activated K-Ras-induced oxidative DNA damage

Seon Ho Park, Jung Jin Kim, Jin Sil Chung, So Ra Lee, Gi Young Lee, Hyung Jung Kim, Young Do Yoo

Research output: Contribution to journalArticlepeer-review

6 Citations (Scopus)


The mutant K-Ras elevates intracellular reactive oxygen species (ROS) levels and leads to oxidative DNA damage, resulting in malignant cell transformation. Ras association domain family 1 isoform A (RASSF1A) is known to play a role as a Ras effector. However, the suppressive effect of RASSF1A on K-RasV12-induced ROS increase and DNA damage has not been identified. Here, we show that RASSF1A blocks K-RasV12-triggered ROS production. RASSF1A expression also inhibits oxidative DNA damage and chromosomal damage. From the results obtained in this study, we suggest that RASSF1A regulates the cellular ROS levels enhanced by the Ras signaling pathway, and that it may function as a tumor suppressor by suppressing DNA damage caused by activated Ras.

Original languageEnglish
Pages (from-to)149-153
Number of pages5
JournalBiochemical and biophysical research communications
Issue number1
Publication statusPublished - 2011 Apr 29


  • DNA damage
  • K-Ras
  • ROS

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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