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Korean Journal of Obstetrics & Gynecology 2008;51(8):858-865.
Published online August 1, 2008.
Apoptosis of the mitochondria protein p32 (gc1qbp) in human ovarian cancer cells.
Miae Won, Sunyoung Lee, Sung Jo Kim, Seongmin Yoon, Kangseok Lee, Jeong Jae Ko, Jeehyeon Bae
1Graduate school of Life Science & Biotechnology, Pochon CHA University School of Medicine, Seongnam, Korea. jeehyeon@cha.ac.kr
2Gynecological Cancer Clinic, Bundang CHA Hospital, Seongnam, Korea.
3Department of Life Science, College of Natural Science, Chung-Ang University, Seoul, Korea.
The purpose of the study was to examine a possible physiological function of p32-mediated apoptosis signaling in ovarian cancer cells. METHODS: SK-OV-3 cells were transfected with respective plasmid DNAs, and cell viability was measured. By immunoprecipitation and immunofluorescence staining analysis, we confirmed that p32 interacts with Harakiri in ovarian cancer cells. RESULTS: In SK-OV-3 cells, p32 interacted with Harakiri and both p32 and Harakiri were colocalized in the mitochondria. In addition, overexpression of p32 induced apoptosis of ovarian cancer cells and augmented Harakiri-mediated apoptosis. CONCLUSION: Our results demonstrated p32 as an apoptosis inducer and helped to provide the better understanding of the function of p32 in ovarian cancer cells and a possibility of p32 in the application of cancer therapeutics.
Key Words: p32, Harakiri, Apoptosis, Cell death, Ovarian cancer

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