喉癌组织中HPV16／18E6、p53和EZH2的表达及其相关性分析

目的 检测HPV16／18E6、p53和EZH2在喉鳞状细胞癌（喉癌）组织中的表达，探讨它们在肿瘤发生发展过程中的相互作用。方法 采用免疫组化En Vision法检测78例喉癌、15例癌旁正常组织、20例声带息肉中HPV16／18E6、p53和EZH2蛋白的表达情况，分析它们的表达与喉癌临床病理特征之间的关系以及三者之间的相关性。结果 喉癌组织、癌旁正常组织、声带息肉中HPV16／18E6蛋白的阳性表达率分别为47.4％（37／78）、20.0％（3／15）和0（0／20）；p53蛋白阳性表达率为60.3％（47／78）、33.3％（5／15）和0（0／20）；EZH2蛋白阳性表达率为65.4％（51／78）、40.0％（6／15）和5.0％（1／20），差异均具统计学意义（P＜0.05）。HPV16／18E6、EZH2的阳性表达率均随肿瘤T分期升高而增高（P＜0.05）；淋巴结转移组HPV16／18E6、p53阳性表达率高于无淋巴结转移组（P＜0.05）；p53阳性表达率随分化程度升高而增高（P＜0.05）。p53和EZH2阳性表达表达一致（kappa值=0.451，P＜0.05）。结论 HPV16／18E6、p53和EZH2蛋白表达与喉癌的发生关系密切。EZH2过表达与p53失活有关，二者在促进喉癌发展过程中发挥重要作用。

The expression of HPV16/18, p53 and EZH2 as well as their correlation in laryngeal squamous cell carcinoma

Objective To study the expression of human papillomavirus 16/18E6（HPV16/18E6）,p53 and EZH2 protein in laryngeal squamous cell carcinoma（LSCC）,and discuss the correlation among them.Methods The expression of HPV16/18E6,p53 and EZ H2 proteins were detected with En Vision immunohistochemical method in 113 cases of paraffin-embedded tissues including 78 LSCC specimens,15 specimens of normal tissue adjacent to cancer and 20 specimens of vocal cord polyp.Their correlations with clinicopathological factors and the interrelation of the expression of HPV16/18E6,p53 and EZH2 proteins in laryngeal cancer were analyzed.Results The positive expression rates of HPV16/18E6,p53 and EZH2 protein in the LSCC group were 47.4％ （37/78）,60.3 ％ （47/78） and 65.4％ （51/78） respectively,which were significantly higher than those in the other groups.The increasing expression of HPV16/18E6 and EZH2 in LSCC was associated with T stage,while p53 and HPV16/18 expression was positively related to lymph node metastases.Additionally,the positive rates of p53 protein in LSCC increased significantly with the increase of histopathological grades.The positive expression of p53 and EZH2 was consistent （kappa =0.451,P ＜ 0.05）.Conclusion Overexpression of HPV16/18E6,p53 and EZH 2 proteins in LSCC contributes to the genesis and development of tumor.Increased expression of EZH2 protein in LSCC may be partly induced by p53 protein inactivation which promote tumor growth and progression.