A critical role for Romo1-derived ROS in cell proliferation

Ah Ram Na, Young Min Chung, Seung Baek Lee, Seon Ho Park, Myeong Sok Lee, Young Do Yoo

Research output: Contribution to journalArticlepeer-review


Low levels of endogenous reactive oxygen species (ROS) originating from NADPH oxidase have been implicated in various signaling pathways induced by growth factors and mediated by cytokines. However, the main source of ROS is known to be the mitochondria, and increased levels of ROS from the mitochondria have been observed in many cancer cells. Thus far, the mechanism of ROS production in cancer cell proliferation in the mitochondria is not well-understood. We recently identified a novel protein, ROS modulator 1 (Romo1), and reported that increased expression of Romo1-triggered ROS production in the mitochondria. The experiments conducted in the present study showed that Romo1-derived ROS were indispensable for the proliferation of both normal and cancer cells. Furthermore, whilst cell growth was inhibited by blocking the ERK pathway in cells transfected with siRNA directed against Romo1, the cell growth was recovered by addition of exogenous hydrogen peroxide. The results of this study suggest that Romo1-induced ROS may play an important role in redox signaling in cancer cells.

Original languageEnglish (US)
Pages (from-to)672-678
Number of pages7
JournalBiochemical and Biophysical Research Communications
Issue number2
StatePublished - May 2 2008


  • Cell proliferation
  • ERK
  • Hydrogen peroxide
  • Reactive oxygen species
  • Romo1

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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