摘要
前期研究表明:IMP3/Ezrin基因是上皮细胞-间质细胞转换(EMT)中的主要构成基因,DEK可以影响结直肠癌细胞的迁移、粘附和侵犯等生物学行为。为了进一步研究DEK与IMP3/Ezrin在结直肠癌中的相关性,首先分析检测了255例结直肠癌和120例癌旁组织蜡块中DEK与IMP3/Ezrin的蛋白水平表达及15例结直肠癌及其癌旁新鲜组织中DEK与IMP3/Ezrin的mRNA水平表达,继而检测结直肠癌细胞中DEK基因敲除前后DEK/IMP3/Ezrin蛋白和mRNA水平变化。结果显示:DEK、IMP3/Ezrin蛋白在255例结直肠癌组织与120例癌旁良性组织中的阳性表达率有明显差异,而15例结直肠癌及癌旁新鲜组织中三种基因mRNA水平以及结直肠癌细胞系中三种基因的蛋白水平也呈现相近的趋势。利用RNAi将DEK进行敲除结果显示:DEK敲除后4种结直肠癌细胞系中的IMP3 mRNA均明显下调,而Ezrin mRNA均明显上调。由此推测,DEK可能通过调节IMP3/Ezrin信号通路相关蛋白促进结直肠癌的演进。
Our previous studies have shown that IMP3/Ezrin gene was the main constitute genes of epithelial - mesenchymal transition （EMT）, and DEK can affect the migration, adhesion and invasion of colorectal cancer cell. In order to study the relationship of DEK and IMP3/Ezrin pathway in colorectal cancer, we examined DEK/ IMP3/Ezrin protein expression levels in 255 cases of colorectal cancer and 120 cases of normal colon tissue, DEK/ IMP3/Ezrin mRNA expression in 15 cases of fresh colorectal tissue, and the IMP3/Ezrin genes in colorectal cancer cell lines knocked down DEK gene. The results showed that there were significant differences between positive expression rates of DEK/IMP3/Ezrin protein in colorectal cancer and benign tissue. Similarly, the genes mRNA levels in the fresh colorectal cancer and colorectal cancer cell lines were also similar trends. After the DEK knocking out from the colorectal cancer cells, IMP3 mRNA were significantly decreased, and Ezrin mRNA were significantly raised. Thus, DEK protein may promote the evolution of colorectal cancer involved in signaling pathways IMP3/ Ezrin.
出处
《辽东学院学报（自然科学版）》
CAS
2016年第3期207-211,223,共6页
Journal of Eastern Liaoning University:Natural Science Edition
基金
2014年辽东学院博士启动基金项目
2015年辽宁省教育厅科学研究一般项目(L2015189)
2015年辽宁省科学技术计划项目(2015020554)
