Abstract: Objective : To elucidate the underlying mechanisms of CIN in oral squamous cell carcinoma. Methods : Seven aneuploidy OSCC cell lines were investigated for the functional status of mitotic checkpoint using FACA to investigate the percentage of cell arrested at G2/M after incubated in nocodazole, and the status of centrosomes in these cell lines was investigated by using double immunofluorescence staining with antibodies against gamma -tubulin and pericentrin. Results : A ll aneu-ploidy OSCC cell lines exhibited high percentages of cell arrested at G2/M phase of the cell cycle after 18 hours incubation in nocodazole, indicating an intact mitotic checkpoint, while centrosome abnormalities, numerical amplification and morphological defect were observed in a fraction of OSCC cells (0.4%~18.8%) in all OSCC cell lines investigated. Conclusion :The CIN phenotype(aneuploidy) in OSCC cells may not attribute to the functional defects of mitotic checkpoint, while the abnormalities of centrosome is likely a contributing factor towards CIN in OSCC cells.