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作 者:谢开红[1] 胡小毛[1] 刘平平 郑力 朱锦灿[3] 刘善淘 何冬梅[3] 刘革修[3]
机构地区:[1]湘南学院附属医院肿瘤科,郴州423000 [2]清华大学第一附属医院血液肿瘤科 [3]暨南大学医学院血液病研究所
出 处:《中华放射医学与防护杂志》2015年第11期801-804,共4页Chinese Journal of Radiological Medicine and Protection
基 金:国家自然基金(81270568)
摘 要:目的研究miR-155在淋巴瘤Raji细胞辐射抵抗中的作用及其机制。方法实时定量聚合酶链反应检测Raji细胞miR-155的表达,CCK-8法检测细胞增殖,流式细胞仪检测细胞凋亡,Westernblot检测PTEN和p-AKT的表达。结果miR-155RNA和p-AKT蛋白在Raji细胞中表达较高,而pten基因mRNA和蛋白质表达水平极低,单纯4.0Gy照射48h后Rajj细胞凋亡率较低;miR-155siRNA不仅使miR-155RNA和p-AKT表达水平明显下降,而且pten基因mRNA和蛋白质水平显著增高,同时细胞显示出增殖抑制作用,显著增加Raji细胞对该辐射剂量敏感性,siRNA+射线照射组细胞凋亡率为(36.78±1.35)%,高于单纯照射组(t=12.572,P〈0.05)。结论miR-155表达对Raji细胞辐射敏感性具有重要影响,其机制与PTEN/PI3K/AKT信号途径激活有关。Objective To investigate the role of miR-155 in radio-resistance of lymphoma cell line Raji cells. Methods The expression of miR-155 was detected by quantitative real-tlme PCR, cell growth was detected by CCK-8 assay, cell apoptosis was detected by flow cytometry, and the protein expressions of PTEN and p-AKT were detected by Western blot. Results The Raji cells had high levels of miR-155 RNA and p-AKT protein had a very low level of PTEN protein. Cell apoptosis was induced by 4. 0 Gy X-ray irradiation after 48 h. The transfection of cells with miR-155 siRNA not only silenced miR-155, but also significantly decreased p-AKT level, increased the expression of pten gene and protein level, inhibited cell proliferation, and increased the radiation sensitivity of Raft cell, the apoptosis rate of siRNA + irradiation group( 36.78% ± 1.35%) was higher than that of irradiation group( t = 12. 572 ,P 〈 0.05 ). Conclusions High levels of miR-155 was involved in radiation resistance of lymphoma Raji cells and this activity is likely modulated by the PTEN/PI3K/AKT signaling pathway.
关 键 词:MIR-155 BURKITT淋巴瘤 辐射
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