凋亡相关蛋白Bcl-XL和Bak在口腔黏膜癌前病变和鳞癌组织中的表达

目的 :探讨凋亡相关蛋白Bcl-XL和Bak在口腔鳞状细胞癌组织发生、发展过程中的表达及意义。方法 :采用免疫组织化学SP法检测 8例正常口腔黏膜上皮、7例异常增生上皮和 4 2例鳞癌组织中Bcl-XL和Bak的表达。结果 :Bcl-XL和Bak在正常黏膜上皮中的表达分别有 12 .5 0 % (1/ 8)阳性率 ;Bcl -XL在鳞癌组织中的表达高于其在正常黏膜与异常增生上皮中的表达 (P <0 .0 5 ) ,差异有显著性 ;Bak在异常增生上皮和鳞癌组织中的表达明显高于正常黏膜 (P <0 .0 5 ) ,但在低分化鳞癌组的表达较高分化组明显降低 (P <0 .0 5 )。结论 :抑凋亡蛋白Bcl-XL上调导致异常增生上皮或 (和 )癌细胞积累。促凋亡因子Bak在代偿性过表达后 ,其作用随癌组织分化程度降低而减弱 ,癌细胞凋亡受限 ,恶性度增强。细胞凋亡的异常调控对口腔鳞癌的发生、发展有重要作用

Expression of Apoptosis-related Proteins Bcl-XL and Bak in Premalignant and Malignant Lesions of the Oral Epithelium

Objective:To investigate the expression and significanc e of apoptosis-related proteins Bcl-XL and Bak during the development and progress ion of oral squamous cell carcinoma(SCC).Methods:8 normal oral epithelia,7 dysplasia epithelia and 42 SCCs were evaluated in immunohistoch emically stained sections for apoptosis regulatory proteins Bcl-XL and Bak.Results:In normal epithelia, the positive rates of Bcl-XL and B ak were both 12.50%(1/8). In SCCs, the positive rate of Bcl-XL was significantly higher than in normal and dysplasia epithelia ( P <0.05).The positive rate of Bak increased significantly in dysplasia epithelia and SCCs (compared with norm al epithelia, P <0.05), and the positive intensity in poorly differentiated SC Cs was lower than in well differentiated SCCs( P <0.05).Conclusions :Up-expression of apoptosis suppressor protein Bcl-XL results in accu mulation of dysplasia and carcinoma cells.Apoptosis is controled due to a decrea se in expression of apoptosis promoter protein Bak after its compensational over -expression.The cooperation of Bcl-XL and Bak results in the progression of SCC. Deregulation of apoptosis could be important to oral carcinogenesis.