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作 者:鲁艳明[1] 孟丽荣[2] 尚超[3] 张淑兰[1]
机构地区:[1]中国医科大学附属盛京医院妇产科,辽宁沈阳110004 [2]澳门理工学院高等卫生学校病理生理教研室,中国澳门000853 [3]中国医科大学神经生物学教研室,辽宁沈阳110001
出 处:《中华肿瘤防治杂志》2011年第8期580-583,共4页Chinese Journal of Cancer Prevention and Treatment
基 金:国家青年科学基金(81001163);澳门特别行政区科学技术发展基金(031/2007/A)
摘 要: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 explore the mechanism of KCC1 regulates the invasion ability of endometrial cancer HEC-1B cells through the extracellular signal-regulated kinase (ERK) signaling pathway. METHODS: The expression of KCC1 and phosphoryla ted ERK1/2 proteins and invasion ability in the HEC-1B cells after peDNA-KCC1 transfeetion were detected by western blot and cell invasion assay. After treatment with U0126, the quantity of p-ERK1/2 and the cell invasion ability were measured again. RE- SULTS: After pcDNA-KCC1 transfeeted to the HEC-1B cells, the expression of KCC1 and p-ERK1/2 increased dramatically (P〈0.05), and the number of cells penetrated filter membrane increased from 26.7±2.3 to 50.3±3.1 (P〈0.05). In HEC-1B cells treated by pcDNA-KCC1 transfection, treatment of U0126 could inhibit phosphorylation of ERK1/2 protein (P〈0.05), and the number of cells penetrated filter membrane decreased from 50.3±3. 1 to 30. 8±5. 9 (P〈0. 05). CONCLUSION: KCC1 gene may be participates in the invasion ability of HEC-1B cells through the ERK signaling pathway.
关 键 词:子宫肿瘤 膜转运蛋白类 丝裂原活化蛋白激酶3 肿瘤浸润
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