Kivi Niina, Rönty Mikko, Tarkkanen Jussi, Auvinen Petri, Auvinen Eeva
Haartman Institute, Department of Virology, University of Helsinki, POB 21 (Haartmaninkatu 3), FIN-00014, Helsinki, Finland.
BMC Clin Pathol. 2012 Aug 3;12:9. doi: 10.1186/1472-6890-12-9.
Cervical cancer is necessarily caused by human papillomaviruses, which encode three oncogenes manifesting their functions by interfering with a number of cellular proteins and pathways: the E5, E6, and E7 proteins. We have earlier found in our microarray studies that the E5 oncogene crucially affects the expression of cellular genes involved in adhesion and motility of epithelial cells.
In order to biologically validate our previous experimental findings we performed immunohistochemical staining of a representative set of tissue samples from different grades of high-risk human papillomavirus associated cervical disease as well as normal squamous and columnar cervical epithelium. Three-dimensional collagen raft cultures established from E5-expressing and control epithelial cells were also examined. The expression of p16, matrix metalloproteinase (MMP) -7, MMP-16, cytokeratin (CK) 8/18, laminin, E-cadherin and beta-catenin was studied.
In agreement with our previous microarray studies, we found intense staining for E-cadherin and beta-catenin in adherens junctions even in high-grade cervical lesions. Staining for MMP-16 was increased in severe disease as well. No significant change in staining for MMP-7 and cytokeratin 8/18 along with the grade of cervical squamous epithelial disease was observed.
Here we have confirmed, using tissue material from human papillomavirus associated lesions, some of the cellular gene expression modifications that we earlier reported in an experimental system studying specifically the E5 oncogene of papillomaviruses. These findings were partially surprising in the context of cervical carcinogenesis and emphasize that the complexity of carcinogenesis is not yet fully understood. Microarray approaches provide a wide overwiev of gene expression in experimental settings, which may yield biologically valid biomarkers for disease diagnostics, prognosis, and follow-up.
宫颈癌必然由人乳头瘤病毒引起,该病毒编码三种癌基因,通过干扰多种细胞蛋白和信号通路发挥作用,即E5、E6和E7蛋白。我们早期在微阵列研究中发现,E5癌基因对参与上皮细胞黏附和运动的细胞基因表达有至关重要的影响。
为从生物学角度验证我们之前的实验结果,我们对不同级别高危人乳头瘤病毒相关宫颈疾病以及正常宫颈鳞状和柱状上皮的代表性组织样本进行了免疫组化染色。还检测了由表达E5的上皮细胞和对照上皮细胞建立的三维胶原筏培养物。研究了p16、基质金属蛋白酶(MMP)-7、MMP-16、细胞角蛋白(CK)8/18、层粘连蛋白、E-钙黏蛋白和β-连环蛋白的表达。
与我们之前的微阵列研究一致,我们发现即使在高级别宫颈病变中,黏附连接处的E-钙黏蛋白和β-连环蛋白也有强烈染色。严重疾病中MMP-16的染色也增加。未观察到MMP-7和细胞角蛋白8/18的染色随宫颈鳞状上皮疾病级别有显著变化。
在此,我们利用人乳头瘤病毒相关病变的组织材料,证实了我们之前在专门研究乳头瘤病毒E5癌基因的实验系统中报道的一些细胞基因表达变化。这些发现在宫颈癌发生的背景下部分令人惊讶,并强调癌症发生的复杂性尚未完全被理解。微阵列方法在实验环境中提供了基因表达的广泛概况,这可能为疾病诊断、预后和随访产生生物学上有效的生物标志物。