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目的:研究KRT17在胃癌组织、细胞的表达及其对上皮间质转化(epithelial mesenchymal transition,EMT)的作用。方法:利用RT-PCR法检测32对配对胃癌及癌旁组织KRT17的表达。用RT-PCR及Western印迹法检测胃癌细胞株与永生化胃黏膜上皮细胞KRT17的表达。免疫组织化学染色法评估227例胃癌组织芯片KRT17表达,结合临床病理资料进行初步分析。Transwell实验观察干扰KRT17的胃癌细胞与对照组细胞迁移、侵袭能力的差异。RT-PCR及Western印迹法检测EMT标志物E钙黏蛋白、波形蛋白的表达。结果 :KRT17在胃癌组织和细胞中表达显著增加,其表达高低与肿瘤组织分级(P=0.008),肿瘤浸润深度(T分期)(P=0.027),淋巴结转移(N分期)(P=0.03)密切相关。干扰KRT17后胃癌细胞迁移和侵袭能力明显下降,E钙黏蛋白的表达明显升高,波形蛋白的表达明显降低。结论:KRT17在胃癌组织中高表达,并与临床病理密切相关。KRT17下调后抑制细胞迁移与侵袭,通过抑制EMT的机制产生作用。
Objective: To investigate the expression of KRT17 in gastric cancer cells and its role in epithelial mesenchymal transition (EMT). Methods: RT-PCR was used to detect the expression of KRT17 in 32 paired gastric cancer tissues and paracancerous tissues. The expression of KRT17 in gastric cancer cell lines and immortalized gastric mucosal epithelial cells was detected by RT-PCR and Western blotting. The expression of KRT17 in 227 gastric cancer tissue samples was evaluated by immunohistochemical staining and analyzed with clinicopathological data. Transwell experiments to observe the interference of KRT17 gastric cancer cells and control cells migration and invasion differences. The expression of EMT marker E cadherin and vimentin were detected by RT-PCR and Western blot. Results: The expression of KRT17 was significantly increased in gastric cancer tissues and cells. The expression of KRT17 was correlated with tumor grade (P = 0.008), tumor invasion depth (T stage) (P = 0.027), lymph node metastasis closely related. The interference of KRT17 gastric cancer cell migration and invasion decreased significantly, E cadherin expression was significantly increased, significantly reduced the expression of vimentin. Conclusion: KRT17 is overexpressed in gastric cancer and closely related to clinicopathologic features. KRT17 downregulation of cell migration and invasion, through the inhibition of EMT mechanism of action.