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. |
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Abstract |
OBJECTIVE 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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