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 journalArticle

46 Citations (Scopus)

Abstract

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
Pages (from-to)672-678
Number of pages7
JournalBiochemical and Biophysical Research Communications
Volume369
Issue number2
DOIs
Publication statusPublished - 2008 May 2

Fingerprint

Cell proliferation
Modulators
Reactive Oxygen Species
Cell Proliferation
Mitochondria
Cells
Cell growth
Neoplasms
MAP Kinase Signaling System
NADPH Oxidase
Growth
Hydrogen Peroxide
Small Interfering RNA
Oxidation-Reduction
Intercellular Signaling Peptides and Proteins
Cytokines

Keywords

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

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

Cite this

A critical role for Romo1-derived ROS in cell proliferation. / Na, Ah Ram; Chung, Young Min; Lee, Seung Baek; Park, Seon Ho; Lee, Myeong Sok; Yoo, Young Do.

In: Biochemical and Biophysical Research Communications, Vol. 369, No. 2, 02.05.2008, p. 672-678.

Research output: Contribution to journalArticle

Na, Ah Ram ; Chung, Young Min ; Lee, Seung Baek ; Park, Seon Ho ; Lee, Myeong Sok ; Yoo, Young Do. / A critical role for Romo1-derived ROS in cell proliferation. In: Biochemical and Biophysical Research Communications. 2008 ; Vol. 369, No. 2. pp. 672-678.
@article{da68a803e1de4be2abb5ee55bec00b3c,
title = "A critical role for Romo1-derived ROS in cell proliferation",
abstract = "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.",
keywords = "Cell proliferation, ERK, Hydrogen peroxide, Reactive oxygen species, Romo1",
author = "Na, {Ah Ram} and Chung, {Young Min} and Lee, {Seung Baek} and Park, {Seon Ho} and Lee, {Myeong Sok} and Yoo, {Young Do}",
year = "2008",
month = "5",
day = "2",
doi = "10.1016/j.bbrc.2008.02.098",
language = "English",
volume = "369",
pages = "672--678",
journal = "The BMJ",
issn = "0730-6512",
publisher = "Kluwer Academic Publishers",
number = "2",

}

TY - JOUR

T1 - A critical role for Romo1-derived ROS in cell proliferation

AU - Na, Ah Ram

AU - Chung, Young Min

AU - Lee, Seung Baek

AU - Park, Seon Ho

AU - Lee, Myeong Sok

AU - Yoo, Young Do

PY - 2008/5/2

Y1 - 2008/5/2

N2 - 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.

AB - 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.

KW - Cell proliferation

KW - ERK

KW - Hydrogen peroxide

KW - Reactive oxygen species

KW - Romo1

UR - http://www.scopus.com/inward/record.url?scp=40849140681&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=40849140681&partnerID=8YFLogxK

U2 - 10.1016/j.bbrc.2008.02.098

DO - 10.1016/j.bbrc.2008.02.098

M3 - Article

VL - 369

SP - 672

EP - 678

JO - The BMJ

JF - The BMJ

SN - 0730-6512

IS - 2

ER -