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目的探讨nectin-4及上皮间质转化(EMT)标志物在胃癌组织中的表达。方法采用RT-PCR和Western blot检测120例胃癌组织及癌旁胃黏膜组织中nectin-4mRNA和蛋白表达。免疫组化检测nectin-4及EMT标志物在120例胃癌组织及癌旁胃黏膜组织中的表达,分析其与胃癌患者临床病理特征的关系。设计靶向nectin-4干扰RNA序列并转染胃癌细胞系SGC7901,Western blot检测转染前后SGC7901细胞中的nectin-4及EMT标志物表达情况,Transwell侵袭实验检测nectin-4对SGC7901细胞侵袭能力的影响。结果 Nectin-4、Snail及波形蛋白(vimentin)在胃癌组织中表达均高于癌旁胃黏膜组织(P<0.05或P<0.01)。上皮型钙黏蛋白(E-cadherin)在胃癌组织中阳性率低于癌旁胃黏膜组织(P<0.01)。Nectin-4表达与胃癌T分期、淋巴结转移及pTNM分期密切相关(P<0.01)。胃癌组织中,nectin-4表达与Snail、vimentin表达呈正相关(r=0.342、0.357,P<0.01),而与E-cadherin表达呈负相关(r=-0.481,P<0.01)。干扰nectin-4表达后,SGC7901细胞中E-cadherin表达上调,Snail及vimentin表达下调(P<0.05),细胞的侵袭能力降低(P<0.05)。结论 Nectin-4在胃癌组织中高表达,并可能通过诱导EMT的发生增强胃癌细胞的侵袭、转移能力。
Objective To investigate the expression of nectin-4 and epithelial-mesenchymal transition (EMT) markers in gastric cancer. Methods The expression of nectin-4 mRNA and protein in 120 gastric cancer tissues and adjacent gastric mucosa tissues were detected by RT-PCR and Western blot. Immunohistochemistry was used to detect the expression of nectin-4 and EMT markers in 120 gastric cancer tissues and adjacent gastric mucosa tissues. The relationship between the expression of nectin-4 and EMT markers and clinicopathological features was analyzed. The siRNA targeting nectin-4 was designed and transfected into gastric cancer cell line SGC7901. Western blot was used to detect the expression of nectin-4 and EMT markers in SGC7901 cells before and after transfection. Transwell invasion assay was used to detect the invasion ability of nectin-4 on SGC7901 cells influences. Results The expression of Nectin-4, Snail and vimentin in gastric cancer tissues were significantly higher than those in adjacent gastric mucosa tissues (P <0.05 or P <0.01). The positive rate of E-cadherin in gastric cancer tissues was lower than that in adjacent gastric mucosa tissues (P <0.01). Nectin-4 expression was closely related to T stage, lymph node metastasis and pTNM stage (P <0.01). The expression of nectin-4 was positively correlated with the expression of Snail and vimentin in gastric cancer (r = 0.342, 0.357, P <0.01), but negatively correlated with the expression of E-cadherin (r = -0.481, P <0.01). After interference of nectin-4 expression, the expression of E-cadherin, the expression of Snail and vimentin in SGC7901 cells were down-regulated (P <0.05), and the invasion ability of cells was decreased (P <0.05). Conclusion Nectin-4 is overexpressed in gastric cancer tissues and may enhance the invasion and metastasis of gastric cancer cells by inducing EMT.