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Molecular and Cellular Biology, August 2005, p. 6603-6616, Vol. 25, No. 15
0270-7306/05/$08.00+0     doi:10.1128/MCB.25.15.6603-6616.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Mitochondrial Ribosomal Protein L41 Suppresses Cell Growth in Association with p53 and p27Kip1

Young A Yoo,1,2 Mi Jin Kim,2,3 Jong Kuk Park,1 Young Min Chung,1 Jong Hyeok Lee,1 Sung-Gil Chi,2 Jun Suk Kim,1,4* and Young Do Yoo3*

Department of Internal Medicine and Division of Brain Korea 21 Program for Biomedical Science, Korea University College of Medicine, Seoul 136-705, South Korea,1 School of Life Science and Biotechnology, Korea University, Seoul 136-705, South Korea,2 Graduate School of Medicine, Korea University College of Medicine, Seoul 136-705, South Korea,3 Department of Internal Medicine, Korea University College of Medicine, Seoul 136-705, South Korea4

Received 18 November 2004/ Returned for modification 5 January 2005/ Accepted 11 May 2005

The p53 protein arrests the cell cycle at the G1 phase when stabilized by the interaction between ribosomal proteins and HDM2 under growth-inhibitory conditions. Meanwhile, p53, when translocated to the mitochondria in response to cell death signals, induces apoptosis via transcription-independent mechanisms. In this report, we demonstrate that the mitochondrial ribosomal protein L41 (MRPL41) enhances p53 stability and contributes to p53-induced apoptosis in response to growth-inhibitory conditions such as actinomycin D treatment and serum starvation. An analysis of MRPL41 expression in paired normal and tumor tissues revealed lower expression in tumor tissue. Ectopic MRPL41 expression resulted in inhibition of the growth of cancer cells in tissue culture and tumor growth in nude mice. We discovered that MRPL41 protein is localized in the mitochondria, stabilizes the p53 protein, and enhances its translocation to the mitochondria, thereby inducing apoptosis. Interestingly, in the absence of p53, MRPL41 stabilizes the p27Kip1 protein and arrests the cell cycle at the G1 phase. These results suggest that MRPL41 plays an important role in p53-induced mitochondrion-dependent apoptosis and MRPL41 exerts a tumor-suppressive effect in association with p53 and p27 Kip1.

* Corresponding author. Mailing address for Young Do Yoo: Graduate School of Medicine, Korea University College of Medicine, Anam Hospital, 126-1, 5ka, Anam-dong, Sungbuk-ku, Seoul 136-705, South Korea. Phone: 82-2-920-5762. Fax: 82-2-920-5762. E-mail: ydy1130{at}korea.ac.kr. Mailing address for Jun Suk Kim: Department of Internal Medicine, Korea University College of Medicine, Seoul 136-705, South Korea. Phone: 82-2-818-6651. Fax: 82-2-920-5762. E-mail: kjs6651{at}kumc.or.kr.

Molecular and Cellular Biology, August 2005, p. 6603-6616, Vol. 25, No. 15
0022-538X/05/$08.00+0     doi:10.1128/MCB.25.15.6603-6616.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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