miR-143增强SKM-1细胞对阿糖胞苷的药物敏感性

miR-143 Enhances Drug Sensitivity of Cytarabine in SKM-1 Cells

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.