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作 者:张红霞[1] 吴广胜[1] ZHANG Hong-Xia WU Guang-Sheng(Department of Rheumatism, the First Affiliated Hospital of Shihezi University Medical College, Shihezi 832000, Chin)
机构地区:[1]石河子大学医学院第一附属医院血液风湿科,石河子832000
出 处:《中国免疫学杂志》2016年第12期1773-1776,共4页Chinese Journal of Immunology
摘 要:目的:探讨β-arrestin1对白血病细胞生物学功能的影响及相关机制的研究。方法:特异性的β-Arrestin1-siRNA和阴性对照siRNA转染K562细胞,形成β-Arrestin1-siRNA组、阴性对照siRNA组和空白组对照组。以此为实验分组,应用transwell小室法检测各组细胞的迁移侵袭能力变化,Western blot检测p STAT3蛋白的表达。结果:β-Arrestin1-siRNA处理组细胞的迁移和侵袭能力较对照组分别下降43%及52%(P<0.05);且p STAT3蛋白表达减少;STAT3抑制剂能抑制K562细胞体外迁移侵袭能力。结论:白血病细胞K562中β-arrestin1蛋白高表达激活STAT3信号通路,从而促进细胞的迁移侵袭能力。Objective: To investigate the function of β-arrestin1 and its related mechanisms in migration and invasion capacity of leukemia cell K562. Methods: β-arrestin1-siRNA or negative siRNA was transfected into K562 cells of experiment group or control group. The migration and invasion capacity of K562 cells was detected by transwell tests; and the protein expression of β-arrestin1 and p STAT3 were detected by Western blot. Results: As compared to control group and negative siRNA group,the migration and invasion capacity of transfected β-arrestin1-siRNA group were attenuated about 43% or 52%( P〈0. 05); Western blot showed that the expression of phosphorylation of STAT3 was decreased in β-arrestin1-siRNA group. And the STAT3 inhibitors obviously suppressed the migration and invasion capacity of K562 cells. Conclusion: In leukemia cells K562,β-arrestin1 activates STAT3 signaling pathway to promote the cell migration and invasion.
关 键 词:β-arrestin1 STAT3 迁移侵袭
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