Mitochondrial reactive oxygen species originating from Romo1 exert an important role in normal cell cycle progression by regulating p27Kip1 expression

Jin Sil Chung, Seung Baek Lee, Seon Ho Park, Sung Tae Kang, Ah Ram Na, Tong Shin Chang, Hyung Jung Kim, Young Do Yoo

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28 Citations (Scopus)


Reactive oxygen species (ROS) steady-state levels are required for entry into the S phase of the cell cycle in normal cells, as well as in tumour cells. However, the contribution of mitochondrial ROS to normal cell proliferation has not been well investigated thus far. A previous report showed that Romo1 was responsible for the high ROS levels in tumour cells. Here, we show that endogenous ROS generated by Romo1 are indispensable for cell cycle transition from G1 to S phase in normal WI-38 human lung fibroblasts. The ROS level in these cells was down-regulated by Romo1 knockdown, resulting in cell cycle arrest in the G1 phase. This arrest was associated with an increase in the level of p27Kip1. These results demonstrate that mitochondrial ROS generated by Romo1 expression is required for normal cell proliferation and it is suggested that Romo1 plays an important role in redox signalling during normal cell proliferation.

Original languageEnglish
Pages (from-to)729-737
Number of pages9
JournalFree Radical Research
Issue number8
Publication statusPublished - 2009 Jul 27



  • Cell cycle arrest
  • Mitochondria
  • p27
  • Reactive oxygen species
  • Redox signalling
  • Romo1

ASJC Scopus subject areas

  • Biochemistry

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