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[目的]探讨体外DNA结合抑制因子(inhibitor of DNA bindingor differentiation,Id)的表达对卵巢上皮癌SKOV3对顺铂化疗敏感性的影响。[方法]构建靶向Id1基因siRNA慢病毒载体并转染SKOV3细胞,筛选出稳定转染的SKOV3细胞克隆。实验分为4组:实验组(Cell+LvshRNA-Id1)、阴性对照组(Cell+Lv-shRNA-NC)、病毒对照组(Cell+Lv-control)与空白对照组(Cell group)。CCK8检测各组SKOV3细胞不同时间增殖活性以及暴露于不同浓度顺铂(0.1、0.2、0.5、1、2、5、10μg/ml)48h后顺铂对各组SKOV3细胞的半数抑制浓度,分析沉默Id1基因后卵巢癌细胞对顺铂化疗敏感性的影响。[结果]三组对照组细胞增殖活性随着时间增加显著,而实验组则增加缓慢。在48h和72h时,实验组细胞增殖活性值分别为0.449±0.072μg/ml、0.885±0.232μg/ml,与三组对照组比较差异均有统计学意义(P均<0.05);实验组顺铂对SKOV3细胞的半数抑制浓度为1.5±0.71μg/ml,明显低于对照组(P<0.01)。[结论]抑制Id1基因表达可以增加顺铂对卵巢癌细胞的生长抑制作用,为临床进一步提高卵巢癌的疗效提供了研究基础。
[Objective] To investigate the effect of in vitro DNA inhibitor (Id) expression on the chemosensitivity of ovarian epithelial carcinoma SKOV3 to cisplatin. [Method] The siRNA lentiviral vector targeting Id1 gene was constructed and transfected into SKOV3 cells. The stably transfected SKOV3 cell clones were screened out. The experiment was divided into 4 groups: experimental group (Cell + LvshRNA-Id1), negative control group (Cell + Lv-shRNA-NC), virus control group (Cell + Lv-control) and blank control group (Cell group). CCK8 was used to detect the proliferation activity of SKOV3 cells in different time groups and the half inhibitory concentration of cisplatin on SKOV3 cells exposed to different concentrations of cisplatin (0.1, 0.2, 0.5, 1, 2, 5, 10μg / ml) Effect of Id1 gene on chemosensitivity to cisplatin in ovarian cancer cells. [Results] The cell proliferation activity of three control groups increased significantly with time, while the experimental group increased slowly. At 48h and 72h, the proliferation activity of the experimental group were 0.449 ± 0.072μg / ml and 0.885 ± 0.232μg / ml, respectively, which were significantly different from those of the three control groups (all P <0.05) The half inhibitory concentration of platinum on SKOV3 cells was 1.5 ± 0.71μg / ml, which was significantly lower than that of the control group (P <0.01). [Conclusion] Inhibition of Id1 gene expression can increase the inhibitory effect of cisplatin on the growth of ovarian cancer cells and provide the basis for further clinical study on the therapeutic effect of ovarian cancer.