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Chromosomal abnormality such as aneuploidy is one of the main factors to cause cancers. This abnormality is caused by defects in centrosomal duplication, and most cancer cells have extra copies of centrosomes, resulting in the formation of multipolar spindles. Several kinases playing in mitotic phase have been implicated in regulating the centrosomal cycle, spindle checkpoint, and chromosome condensation and segregation. They also have the ability to act as oncogenes. For studying the relationship between mitotic kinase and oral cancers, the kinase activity of polo-like kinase-1, which is one of mitosis-specific kinases, is analyzed in oral carcinoma cells originated differently. Kinase activity was increased in these cancer cells compared to normal human gingival fibroblast primary cultured cells. Moreover, the mitotic cell populations were also increased in these cell lines. Whereas the inhibition of Polo-like kinase-1 by C-terminal domain in human gingival fibroblast cells induced multiploidy, the apoptotic cell population was increased in oral cancer cells overexpressed C-terminal domain of Polo-like kinase-1. These data suggested that polo-like kinase-1 might be involved in the oncogenic effect in oral cancer like other solid human carcinomas, and be target molecules for anti-cancer drug.