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目的:研究凋亡相关基因Fas、FasL及Bcl-2蛋白在口腔黏膜异常增生上皮及鳞癌组织中变化规律。方法:采用免疫组织化学SP法检测口腔黏膜异常增生上皮及鳞癌组织中凋亡相关基因Fas、FasL及Bcl-2蛋白表达。结果:发现Fas表达水平无差异,但Fas染色在正常、单纯性增生、轻度异常增生组织中以胞膜型为主,而原位癌及鳞癌组织中以胞浆型为主,中度异常增生时两型兼有;FasL在鳞癌组织中过度表达,与对照组、单纯增生组比较差异显著(P<0.05),FasL表达与局部浸润的淋巴细胞呈负相关(r=-0.437,P<0.05)。Bcl-2表达在原位癌时出现高峰,与对照组、单纯增生组比较差异显著(P<0.05),Bcl-2表达水平与Fas L表达水平相关显著(r=0.337,P<0.05)。结论:Fas、FasL及Bcl-2参与了口腔癌前病变癌变发生发展过程,作用的机制可能是它们分别或协同作用抑制细胞凋亡、延长异常细胞生存期、利于免疫逃逸,为细胞癌变提供了条件。
OBJECTIVE: To study the changes of Fas, FasL and Bcl-2 protein in epithelial and squamous cell carcinoma of oral mucosa with abnormal proliferation. Methods: Immunohistochemical SP method was used to detect the expression of Fas, FasL and Bcl-2 proteins in the epithelial and squamous cell carcinomas of oral mucosa. Results: There was no difference in the expression level of Fas, but Fas staining was mainly in membrane type in normal, simple hyperplasia and mild dysplasia tissues, but mainly in cytoplasm, FasL was overexpressed in squamous cell carcinoma with significant difference (P <0.05) compared with control group and simple hyperplasia group (P <0.05). The expression of FasL was negatively correlated with lymphocytes locally infiltrated (r = -0.437, P <0.05). The expression of Bcl-2 protein was significantly higher in Fas group (r = 0.337, P <0.05). The expression of Bcl-2 protein was significantly higher than that in control group and simple hyperplasia group (P <0.05). Conclusions: Fas, FasL and Bcl-2 are involved in the carcinogenesis and progression of oral precancerous lesions. The mechanism may be that they inhibit apoptosis individually, prolong the survival of abnormal cells, facilitate immune escape and provide a condition.