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机构地区:[1]重庆医科大学分子医学与肿瘤研究中心,重庆400016
出 处:《重庆医科大学学报》2017年第11期1411-1416,共6页Journal of Chongqing Medical University
摘 要:目的:研究8-氯腺苷(8-chloro-adenosine,8-Cl-Ado)对乳腺癌SK-BR-3细胞增殖和迁移的影响,以及与RNA编辑酶1(adenosine deaminases acting on RNA 1,ADAR1)表达的相关性。方法:蛋白印迹实验检测乳腺癌组织中ADAR1的蛋白表达量以及8-Cl-Ado(10μmol/L)处理乳腺癌SK-BR-3细胞不同时间ADAR1蛋白表达量的变化;MTT法和形态学观察检测不加药组和8-Cl-Ado(10μmol/L)加药组对SK-BR-3细胞增殖的影响;MTT法和伤口愈合实验检测SK-BR-3细胞过表达ADAR1质粒(空白对照组、空载组、ADAR1-P110组、ADAR1-P150组)对8-Cl-Ado作用SK-BR-3细胞增殖及迁移的影响。结果:乳腺癌癌组织中ADAR1-P110和ADAR1-P150蛋白表达量均明显高于癌旁组织(t=9.871,P=0.000;t=7.169,P=0.000);8-Cl-Ado作用SK-BR-3细胞48 h后ADAR1-P110和ADAR1-P150蛋白表达量均明显降低(t=-8.838,P=0.013;t=-19.866,P=0.003);8-Cl-Ado作用SK-BR-3细胞ADAR1-P110组和ADAR1-P150组48 h后增殖抑制率均明显低于空白组(P均为0.000);8-Cl-Ado作用SK-BR-3细胞ADAR1-P110组和ADAR1-P150组48 h后的迁移率均明显高于空白组(P均为0.000)。结论:8-Cl-Ado能明显抑制SK-BR-3细胞增殖和迁移,其作用机制可能与ADAR1的表达下调有关。Objective:To evaluate the effects of 8-chloro-adenosine (8-C1-Ado) on proliferation, migration and adenosine deaminases acting on RNA 1 (ADAR1) expression of SK-BR-3 breast cancer cells. Methods:The expression of ADAR1 protein in breast cancer tissues and SK-BR-3 cells treated by 8-C1-Ado(10 μmol/L) at different time were evaluated by Western blot. The effects of 8-C1- Ado(10 μmol/L) on proliferation of SK-BR-3 at different time were detected by MTr and morphology observation. The effects of ADAR1 plasmid over-expression on proliferation and cell metastasis in SK-BR-3 cells(the blank group, the vector group, the ADAR1-P110 group,the ADARI-P150 group) were tested by MTF and wound healing assay. Results:The expressions of ADARI- P110 and ADAR1-P150 protein in breast cancer tissues were significantly higher than those in adiacent tissues(t=9.871 ,P=0.000;t= 7.169,P=0.000) and decreased obviously in SK-BR-3 cells treated by 8-C1-Ado after 48 hours(t=-8.838,P=0.013;t=-19.866,P= 0.003). The proliferation inhibition rates of SK-BR-3 cells treated by 8-C1-Ado after 48 hours in the ADAR1-P110 group and the ADAR1-P150 group were lower than those in the control group(All P=0.000). Furthermore,the migration rates of SK-BR-3 cells treated by 8-C1-Ado after 48 h in the ADAR1-P110 group and the ADAR1-P150 group were higher than those in the control group (All P〈0.000). Conclusion:8-C1-Ado could inhibit the proliferation and migration of SK-BR-3 breast cancer cells by the down- regulation of the expression of ADAR1 protein,the mechanism of action may be related to the down-regulation of ADAR1 protein ex presslon
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