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.