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目的观察BCL6共抑制因子样蛋白1(BCORL1)在非小细胞肺癌(NSCLC)组织中的表达,并通过下调肺癌A549细胞中BCORL1的水平观察对A549细胞侵袭和迁移能力的影响。方法收集68例NSCLC组织及对应的癌旁组织,应用免疫组织化学染色分析BCORL1和E钙黏素(E-cadherin)在NSCLC及对应癌旁组织中的表达;采用小干涉RNA(siRNA)下调肺癌A549细胞中BCORL1的水平,TranswellTM小室法检测A549肺癌细胞迁移和侵袭能力。结果 BCORL1蛋白在NSCLC组织中表达水平显著高于对应癌旁组织,而E-cadherin蛋白在NSCLC组织中表达水平则显著低于对应癌旁组织;相关性分析证实BCORL1蛋白与E-cadherin蛋白在NSCLC组织中的表达呈显著负相关;临床相关分析发现BCORL1蛋白表达与淋巴结转移和TNM分期具有显著的相关性;特异性siRNA下调BCORL1水平后,E-cadherin蛋白上调;敲低BCORL1后,明显抑制A549肺癌细胞侵袭和迁移。结论 BCORL1在NSCLC组织中高表达且与E-cadherin表达呈显著负相关,其高表达与NSCLC恶性临床病理特征相关。敲低BCORL1,上调E-cadherin表达并抑制肺癌细胞侵袭和迁移能力。
Objective To observe the expression of BCL6 costimulatory protein 1 (BCORL1) in non-small cell lung cancer (NSCLC) and to observe the effect of BCORL1 on the invasion and migration of A549 cells by down-regulating the expression of BCORL1 in A549 cells. Methods The expression of BCORL1 and E-cadherin in non-small cell lung cancer (NSCLC) and their corresponding paracancerous tissues was detected by immunohistochemical staining in 68 NSCLC tissues and their corresponding paracancerous tissues. Lung cancer was down-regulated by siRNA The level of BCORL1 in A549 cells and the ability of migration and invasion of A549 lung cancer cells were detected by TranswellTM chamber method. Results The expression of BCORL1 protein in NSCLC tissues was significantly higher than that in paracancerous tissues, while the expression of E-cadherin protein in NSCLC tissues was significantly lower than that in corresponding paracancerous tissues. Correlation analysis confirmed that BCORL1 protein and E-cadherin protein in NSCLC There was a significant negative correlation between the expression of BCORL1 protein and lymph node metastasis and TNM staging. The downregulation of BCORL1 protein by specific siRNA down-regulated the expression of E-cadherin protein. The knockdown of BCORL1 significantly inhibited the expression of A549 Lung cancer cell invasion and migration. Conclusion BCORL1 is highly expressed in NSCLC tissues and has a significant negative correlation with E-cadherin expression. The high expression of BCORL1 is associated with the clinicopathological features of NSCLC. Knockdown of BCORL1 upregulates E-cadherin expression and inhibits lung cancer cell invasion and migration.