中文摘要：

目的：分析STK15及p53蛋白表达与口腔鳞状细胞癌（OSCC）中心体扩增相关性，探讨OSCC中心体扩增可能分子调控机制。方法：8例正常口腔黏膜及43例OSCC石蜡包埋组织，采用间接免疫荧光双重染色了解OSCC中心体数目扩增状况，采用免疫组织化学方法检测相应组织 p53、STK15蛋白表达情况，并分析其与中心体扩增相关性。结果：中心体扩增可见于76.74%（33/43）OSCC中。OSCC中STK15阳性率为67.44%（29/43），STK15阳性率在p53阳性组高于p53阴性组（P〈0.05）。 OSCC中心体扩增发生率在STK15/p53阳性共表达组高于STK15/ p53阴性组（P〈0.05），Spearman相关分析显示STK15/ p53阳性共表达与OSCC中心体扩增之间存在相关关系（r=0.356，P=0.019）。结论：中心体扩增是OSCC常见异常现象，p53/STK15转激活-非依赖通路可能参与中心体异常的形成，与之共同参与OSCC的发生。

英文摘要：

Objective： This study proposed a possible molecular mechanism underlying centrosome amplification in oral squa-mous cell carcinoma （OSCC） by analyzing the relationship of centrosome amplification with the expression of STK15 and p53 in OS-CC tissues. Methods： The expression of STK15 and p53 in formalin-fixed, paraffin-embedded tissues from 8 patients with normal oral epithelium and 43 with OSCC were quantitatively analyzed by immunohistochemistry. Centrosome status was investigated by an indi-rect-immunofluorescence double-staining method to determine the message of centrosome amplification in OSCC. The correlation of the expression of the two proteins with centrosome amplification in OSCC was statistically analyzed with SPSS13.0. Results： Normal oral epithelium showed normal centrosomes in epithelium cells, whereas 33 of the 43 OSCC cases （76.74%） showed evidence of centro-some amplification. STK15 was undetectable in normal oral epithelium. The percentage of STK15 overexpression was 67.44% in OS-CC （P=0.028）. The percentage of STK15 overexpression was significantly higher in OSCC with positive p53 staining than in OSCC with negative p53 staining （P=0.01）. Spearman correlation analysis indicated a correlation between STK15/p53 positive co-expression and centrosome amplification of OSCC （P=0.019）. Conclusion： Centrosome amplification is a common abnormal phenomenon in OS-CC. The p53/STK15 trans-activation-independent pathway plays a role in the systemic molecular regulation of centrosome in OSCC, which leads to the occurrence of OSCC.