BMB Rep. 2010; 43(1): 057-061  
Over-expression of JunB inhibits mitochondrial stress and cytotoxicity in human lymphoma cells exposed to chronic oxidative stress
Young-Ok Son1,#, Jung-Sun Heo2,#, Tae-Geum Kim3, Young-Mi Jeon2, Jong-Ghee Kim2 & Jeong-Chae Lee2,3,*
1Graduate Center for Toxicology, University of Kentucky, Lexington, Kentucky 40536-0001, USA, 2Institute of Oral Biosciences and BK 21 Program, 3Department of Bioactive Material Sciences and Research Center of Bioactive Materials, Chonbuk National University, Jeonju 561-756, Korea
Correspondence to: Tel: 82-63-270-4049; Fax: 82-63-270-4049; E-mail:
Received: August 3, 2009; Accepted: October 7, 2009; Published online: January 31, 2010.
© Korean Society for Biochemistry and Molecular Biology. All rights reserved.

Activator protein-1 can induce either cell survival or death, which is controlled by opposing effects of different Jun members. It is generally accepted that c-Jun is pro-apoptotic, but that JunD is anti-apoptotic in stress-exposed cells. Additionally, although there are reports suggesting that JunB plays a protective role, its role in stress-induced apoptosis remains unclear. Here, we investigated the role of JunB in H(2)O(2)-induced cell death using cells that over-expressed the protein or were transfected with si-JunB. Inhibition of JunB expression accelerated H(2)O(2)-mediated loss of mitochondrial membrane potential (MMP) and cytotoxicity. Conversely, over-expression of JunB protein led to significant inhibition of the MMP loss and cell death. The increase in JunB expression also attenuated nuclear relocation of apoptosis-inducing factor and mitochondrial Bcl-2 reduction that occurred following H(2)O(2) exposure. These results suggest that JunB can signal survival against oxidant-mediated cell death by suppressing mitochondrial stress.
Keywords: Human lymphoma cells, Hydrogen peroxide, JunB, Mitochondrial stress, Oxidative stress

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