口腔鳞状细胞癌细胞周期蛋白E表达与中心体扩增相关性

Cyclin E overexpression and centrosome amplification in squamous cell carcinoma of oral cavity

目的了解口腔鳞状细胞癌细胞周期蛋白E(cyclin E)表达与中心体扩增相关性,探讨其中心体扩增的可能分子机制。方法正常口腔黏膜组织12例,不同分化程度的口腔鳞状细胞癌46例石蜡包埋组织,采用间接免疫荧光双重染色(γ-微管蛋白单克隆抗体及细胞角蛋白多克隆抗体)观察口腔鳞状细胞癌中心体扩增状况;采用免疫组织化学(SABC法)检测相应组织cyclin E蛋白表达情况.分析cyclin E蛋白表达与中心体扩增之间的相关性。结果中心体扩增可见于80.4%(37/46)口腔鳞状细胞癌组织中,而cyclin E蛋白过表达可在65.2%(30/46)的口腔鳞状细胞癌组织中见到;中心体扩增发生率在cyclin E阳性组为90.0%(27/30),而在cyclin E蛋白阴性组为10/16,两组间差异有统计学意义(X^2=5.014,P<0.05);Spearman相关分析显示中心体扩增与cyclin E蛋白阳性表达间存在相关关系(r=0.330,P<0.05);绝对危险度分析OR值为5.400(1.130,25.809)。结论肿瘤细胞中心体循环调控可能是一个多因素参与的复杂过程,cyclin E蛋白表达的高调作为危险因素之一可能在口腔鳞状细胞癌中心体扩增中起一定作用。

Objective To study the correlation between cyclin E protein overexpression and centrosome amplification in oral squamous cell carcinoma （OSCC）. Methods Formalin-fixed, paraffinembedded tissues from 12 normal oral epithelium cases and 46 cases of OSCC were studied. Their centrosome status was analyzed by indirect immunofluorescence double staining with antibodies to centrosome protein gamma-tubulin and cytokeratin. The expression of cyclin E protein was studied by immunohistocbemical methods. The correlation between cyclin E protein expression and centrosome amplification in OSCC was statistically analyzed by SPSS 12. 0. Results Thirty-seven of the 46 OSCC cases （ 80. 4% ） studied showed evidence of centrosome amplification, as signified by enlargement and/or increase in number of centrosomes, while normal oral epithelium possessed centromeres of normal size and number. Positive staining for cyclin E protein was observed in 30 of the 46 OSCC cases （ 65.2% ）, while all the normal oral epithelium cases were cyclin E protein-negative. The percentage of centrosome amplification in OSCC with positive cyclin E protein staining （90. 0%, 27/30） was higher than that in OSCC with negative cyclin E protein staining （62.5%, 10/16） （ X^2 = 5. 014, P 〈 0. 05）. Centrosome amplification showed positive correlation with cyclin E protein overexpression （ r = 0. 330, P 〈 0. 05 ）. Conclusion Up-regulation of cyclin E protein may represent one of the possible mechanisms for centrosome amplification in OSCC.