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J. Biol. Chem., Vol. 280, Issue 47, 39485-39492, November 25, 2005

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Mitochondrial Manganese-Superoxide Dismutase Expression in Ovarian Cancer

ROLE IN CELL PROLIFERATION AND RESPONSE TO OXIDATIVE STRESS^*

Yumin Hu12, Daniel G. Rosen1, Yan Zhou, Li Feng, Gong Yang, Jinsong Liu, and Peng Huang3

From the Departments of Molecular Pathology and Pathology, The University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030

Superoxide dismutases (SODs) are important antioxidant enzymes responsible for the elimination of superoxide radical (). The manganese-containing SOD (Mn-SOD) has been suggested to have tumor suppressor function and is located in the mitochondria where the majority of is generated during respiration. Although increased reactive oxygen species (ROS) in cancer cells has long been recognized, the expression of Mn-SOD in cancer and its role in cancer development remain elusive. The present study used a human tissue microarray to analyze Mn-SOD expression in primary ovarian cancer tissues, benign ovarian lesions, and normal ovary epithelium. Significantly higher levels of Mn-SOD protein expression were detected in the malignant tissues compared with normal tissues (p < 0.05). In experimental systems, suppression of Mn-SOD expression by small interfering RNA caused a 70% increase of superoxide in ovarian cancer cells, leading to stimulation of cell proliferation in vitro and more aggressive tumor growth in vivo. Furthermore, stimulation of mitochondrial production induced an increase of Mn-SOD expression. Our findings suggest that the increase in Mn-SOD expression in ovarian cancer is a cellular response to intrinsic ROS stress and that scavenging of superoxide by SOD may alleviate the ROS stress and thus reduce the simulating effect of ROS on cell growth.

Received for publication, March 25, 2005 , and in revised form, September 1, 2005.

^* This study was supported in part by Grants CA85563, CA100428, and CA109041 (to P. H.) from the NCI, National Institutes of Health, and RSG-04-028-1-CCE (to J. L.) from the American Cancer Society. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ These authors contributed equally to this work.

² Recipient of the Rosalie B. Hite Fellowship.

³ To whom correspondence should be addressed: Dept. of Molecular Pathology, Box 089, The University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Blvd., Houston, TX 77030. Tel.: 713-792-7742; Fax: 713-794-4672; E-mail: phuang{at}mdanderson.org.

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