论文部分内容阅读
目的:探讨K-CL共转运体(KCC)1基因在调节子宫内膜癌侵袭能力的过程中与细胞外信号调节激酶(ERK)转导途径相互作用机制。方法:将pcDNA-KCC1表达载体转染子宫内膜癌HEC-1B细胞,蛋白质印迹法检测KCC1、p-ERK1/2表达的变化;Transwell侵袭小室检测细胞侵袭能力的变化;ERK抑制剂U0126处理转染后的细胞,再通过上述方法检测p-ERK1/2表达及细胞侵袭能力的变化。结果:转染pcDNA-KCC1表达载体后,转染组细胞KCC1、p-ERK1/2蛋白表达明显上调(P<0.05),侵袭至滤膜下的细胞数由26.7±2.3增加到50.3±3.1,P<0.05;应用ERK抑制剂U0126处理实验组后,p-ERK1/2蛋白表达明显下调,侵袭至滤膜下的细胞数由50.3±3.1降低到30.8±5.9,P<0.05。结论:KCC1通过参与ERK信号转导途径调节子宫内膜癌细胞的侵袭能力。
Objective: To investigate the mechanism of interaction between K-CL co-transporter (KCC) 1 gene and extracellular signal-regulated kinase (ERK) transduction pathway in regulating the invasion of endometrial carcinoma. Methods: The expression of KCC1 and p-ERK1 / 2 was detected by western blotting in transfected endometrial carcinoma HEC-1B cells with pcDNA-KCC1 expression vector; the invasion ability of cells was detected by Transwell invasion chamber; the expression of ERK inhibitor U0126 Dyed cells, and then by the above method to detect p-ERK1 / 2 expression and cell invasion ability changes. Results: The expression of KCC1 and p-ERK1 / 2 in transfected cells was significantly up-regulated (P <0.05) after transfected with pcDNA-KCC1. The number of cells infiltrating into the membrane increased from 26.7 ± 2.3 to 50.3 ± 3.1, P <0.05. The expression of p-ERK1 / 2 was significantly down-regulated after treatment with ERK inhibitor U0126, and the number of cells infiltrating the filter decreased from 50.3 ± 3.1 to 30.8 ± 5.9 (P <0.05). Conclusion: KCC1 regulates the invasiveness of endometrial cancer cells by participating in the ERK signal transduction pathway.