摘要
目的:通过了解丝氨酸/苏氨酸激酶15(STK15)及蛋白质53(p53)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OSCC发生发展中的作用及意义.材料与方法:正常口腔黏膜8例,上皮异常增生组织27例,口腔鳞状细胞癌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,分析其在各组间的差异及其临床病理学意义.结果:STK15在正常口腔黏膜阴性表达,在上皮异常增生组及OSCC中阳性表达率分别为40.74%(11/27)、67.44%(29/43),其阳性表达率在各组间的差异均有统计学意义(P<0.05).p 53在正常口黏膜阴性表达,在上皮异常增生组及OSCC中阳性表达率分别为37.04%(10/27)、48.84%(21/43),与正常组相比差异均有统计学意义(P<0.05),OSCC与异常增生组相比差异无统计学意义(P>0.05).在正常口腔黏膜、上皮异常增生及OSCC中STK15和p53同时阳性表达率分别为0%(0/8)、18.52%(5/27)、41.86%(18/43),各组间差异均有统计学意义(P<0.05).OSCC中STK15)阳性表达率在p53阳性表达组和p53阴性表达组分别为85.71%(18/21)、50%(11/22),两组间比较差异有统计学意义(P<0.05).STK15、p53阳性表达率在OSCC伴有淋巴结转移组高于不伴淋巴结转移组,且差异有统计学意义(P<0.05).结论:①STK15过表达是口腔黏膜癌变过程的早期事件并且可能与口腔癌发生进程有关.②同时发生突变型p53和STK15表达增高可能在OSCC发生中有意义,从异常增生最终演变成鳞癌可能有二者协同作用的参与.③STK15过表达对OSCC淋巴结转移有影响,可能成为判断OSCC预后的重要指标之一.
Objective： To investigate the expression of STK15 and p53 proteins in oral precancerous lesions and oral squamous cell carcinomas （ 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 case of dysplasia with different degree epithelium dysplasia and 43 cases of OSCC with different differentiation were investigated for the expression of p53 and STK15 by using Immtmohistochemistry. The change trends, clinical and pathological significance of the expressions of these two proteins were statistical analyzed by SPSS12.0. Results： STK15 and p53 were not detectable in normal oral epithelium and both significantly altered from mile - dysplasia epithelium to OSCC. The percentage of STK15 over - expression were 40.74% （ 11/27 ） in epithelial dysplasia and 67.44% （29/43） in OSCC （ P = 0. 028 ）, while the percentage of positive p53 expression were 37.04% （ 10/27 ） in epithelial dysplasia and 48.84% （21/43） in OSCC respectively （P = 0. 333 ）. The percentages of eoexpression of these two proteins were 0% （0/8） in normal oral epithelium, 18.52% （5/27） in dysplasia,41.86% （18/43） in OSCC （P 〈0. 05 for all）. The percentage of STK15 over - expression in OSCC with positive p53 staining was significantly higher than that in OSCC with negative p53 staining （ P = 0.012 ）. Both STK15 over - expression and p53 positive staining were significantly associated with regional lymph node involvement （P 〈0.05 for all） , while no correlation were found for protein expressions and tumor differentiation, as well as TNM stages. Conclusion： （1） STK15 up - regulation was an early event in oral carcinogenesis and that might be related with the progression of OSCC. （2）Simultaneously increased expression of mutant p53 and STK15 occurred in OSCC meaningful, suggested P53 and STK15 is the result of synergies from dysplasia into OS
出处
《贵州科学》
2007年第B05期400-406,共7页
Guizhou Science
