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作 者:崔佳奇 邓琳丽 王利[1] Cui Jiaqi;Deng Linli;Wang Li(Department of Hematology,The First Affiliated Hospital of Chongqing Medical University,Chongqing 400016,China)
机构地区:[1]重庆医科大学附属第一医院血液科,重庆400016
出 处:《中国细胞生物学学报》2018年第7期1153-1158,共6页Chinese Journal of Cell Biology
基 金:国家自然科学基金(批准号:81250034);重庆市教委基金(批准号:KJ1702017)资助的课题~~
摘 要:该文探讨了miR-143增强SKM-1细胞对阿糖胞苷(cytarabine,Ara-C)的药物敏感性以及其相应机制。采用CCK-8法筛选出Ara-C干预的最佳条件。采用流式细胞仪检测细胞周期和凋亡率。采用Western blot检测Akt、p Akt蛋白表达水平。结果显示,过表达miR-143联合Ara-C组的细胞凋亡率(88.50%)显著高于空病毒对照联合Ara-C组(67.47%)及过表达miR-143组(31.01%),差异具有统计学意义(P<0.05)。过表达miR-143联合Ara-C组G1期的细胞比例(87.24±6.12)%显著高于空病毒对照联合Ara-C组(72.10±3.71)%和过表达miR-143组(57.73±5.02)%,呈现较明显的G1期阻滞。过表达miR-143+Ara-C组的p Akt蛋白相对表达量相比于空病毒对照+Ara-C组和过表达miR-143组明显降低(P<0.05),而各组Akt蛋白相对表达量无明显差异(P>0.05)。以上结果表明,过表达miR-143能够提高SKM-1细胞对阿糖胞苷的药物敏感性,其机制可能与通过降低Akt蛋白磷酸化水平有关。The aim of this study was to investigate whether miR-143 could enhance the drug sensitivity of cytarabine(Ara-C) in SKM-1 cells and the corresponding mechanism. The CCK-8 method was used to screen out the best conditions for Ara-C intervention. The cell cycle and apoptosis rate were measured by flow cytometry. Western blot was used to detect the expression of Akt and p Akt protein. The results showed that the LV-hsa-miR-143+Ara-C group was significantly higher(88.50%) than the LV-control+Ara-C group(67.47%) and LV-hsa-miR-143(31.01%)(P0.05). The percentage of cells in G1 phase of LV-hsa-miR-143+Ara-C group(87.24±6.12)% was significantly higher than that in LVcontrol+Ara-C group(72.10±3.71)% and LV-hsa-miR-143 group(57.73±5.02)%, showing obvious G1 arrest. The relative expression of p Akt protein in LV-hsa-miR-143+Ara-C group was significantly lower than that in LV-control+Ara-C group and LV-hsa-miR-143 group(P0.05). There was no significant differences in the relative expression of Akt protein in each group(P0.05). The above results indicate that overexpression of miR-143 can increase the drug sensitivity of cytarabine in SKM-1 cells. The mechanism may be related to the decrease of Akt phosphorylation.
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