口腔黏膜癌变过程中丝氨酸/苏氨酸激酶15的表达及意义  

The over-expression of serine/threonine kinase 15 protein in oral carcinogenesis

作　　者：卢虹[1] 蔡扬[1] 于燕妮[2] 杨宏[1] 

机构地区：[1]贵阳医学院附属医院口腔内科,贵州贵阳550004 [2]贵阳医学院附属医院病理科,贵州贵阳550004

出　　处：《华西口腔医学杂志》2009年第1期88-91,共4页West China Journal of Stomatology

基　　金：国家自然科学基金资助项目(30460139);教育部留学回国人员科研启动基金资助项目(N2005-1)

摘　　要：目的了解丝氨酸/苏氨酸激酶15(STK15)在口腔黏膜癌变过程中的表达变化,探讨P53/STK15转激活-非依赖通路在口腔鳞癌(OSCC)发生发展中的作用及意义。方法正常口腔黏膜8例,上皮异常增生患者27例,OSCC患者43例,石蜡包埋组织,采用免疫组化SABC法了解STK15及P53蛋白表达情况,分析二者的相关性及其临床病理学意义。结果STK15在正常口腔黏膜无表达,在上皮异常增生及OSCC中阳性率分别为40.74%(11/27)和67.44%(29/43),各组间差异均有统计学意义(P<0.05);口腔鳞癌中STK15阳性率在P53阳性组高于P53阴性组,在OSCC有淋巴结转移组高于无淋巴结转移组,差异均有统计学意义(P<0.05)。结论STK15过表达是口腔黏膜癌变过程的早期事件,口腔鳞癌STK15过表达可能与p53突变有关并与OSCC淋巴结转移密切相关,P53/STK15转激活-非依赖通路在OSCC发生发展中可能起重要作用。Objective To investigate the expression of STK15 and P53 proteins in oral precancerous lesions and oral squamous cell carcinoma （OSCC） and elucidate the possible role of P53/STK15 switch activation-independent pathway in oral carcinogenesis. Methods Formalin-fixed, paraffin-embedded tissues of 8 cases of normal oral epithelium, 27 cases of dysplasia with different degree epithelium dysplasia and 43 cases of OSCC with different differentiation were investigated for the expression of STK15 and P53 proteins by using immunohistochemistry. The clinical and pathological significance of STK15 over-expression in oral carcinogenesis were statistically analyzed by SPSS 12.0. Results STK15 protein was not detectable in normal oral epithelium and significantly altered from mild- dysplasia to OSCC. The percentage of STK15 over-expression were 40.74%（11/27） in dysplasia and 67.44%（29/43） in OSCC （P〈0.05）. The percentage of STK15 over-expression in OSCC with positive P53 staining was significantly higher than that in OSCC with negative P53 staining （P〈0.05）. STK15 over-expression was significantly associated with regional lymph node involvement（P〈0.05）, while no correlation was found for STK15 over-expression and tumor differentiation, as well as TNM stages. Conclusion STK15 up-regulation was an early event in oral carcinogenesis. The up-regulation of STK15 protein in OSCC may partly result from p53 mutations, which probably contribute a role in lymph node metastasis of OSCC as well. P53/STK15 switch activation-independent pathway may play some roles in oral carcinogenesis.

关 键 词：丝氨酸/苏氨酸激酶15 癌前损害 异常增生 鳞状细胞癌 

分 类 号：R739.8[医药卫生—肿瘤]