| 夏凤君,申铁兵.细胞信号转导抑制因子1沉默增强人口腔癌细胞对化疗药物的敏感性[J].安徽医药,2016,20(8):1544-1547. |
| 细胞信号转导抑制因子1沉默增强人口腔癌细胞对化疗药物的敏感性 |
| Effects of suppressor of cytokine signaling-1 silencing on the chemotherapeutic drugs sensitivity of human oral cancer |
| 投稿时间：2016-04-05 |
| DOI： |
| 中文关键词: 口腔肿瘤 细胞因子信号转导蛋白抑制因子 基因沉默 氟尿嘧啶 长春新碱 |
| 英文关键词: Mouth neoplasms Suppressor of cytokine signaling proteins Gene silencing Fluorouracil Vincristine |
| 基金项目: |
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| 摘要点击次数: 2568 |
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| 中文摘要: |
| 目的研究细胞因子信号转导抑制因子1(SOCS1)基因沉默对人口腔癌细胞化疗药物敏感性的影响及相关机制。方法 Western blotting及实时荧光定量(PCR)验证SOCS1干扰序列沉默人口腔表皮样癌细胞(KB细胞)株中SOCS1的表达水平；MTT比色法分析细胞对化疗药物敏感性的变化；流式细胞术检测细胞凋亡。结果 将SOCS1干扰片段转染KB细胞后,SOCS1 mRNA及蛋白表达水平均明显降低。沉默SOCS1表达后,化疗药物5-氟尿嘧啶和长春新碱对KB细胞的半数抑制浓度(IC50)均显著变小(P<0.05),SOCS1沉默还可增加长春新碱诱导的细胞凋亡(P<0.05),SOCS1表达抑制后KB细胞核转录因子-κB(NF-κB)和半胱氨酸天冬氨酸蛋白酶-3(Caspase-3)的蛋白表达水平明显降低,与对照组比较差异均有统计学意义(P<0.05)。结论 SOCS1表达有效抑制后,人口腔癌细胞KB对化疗药物的敏感性增强,且促进化疗药物诱导的肿瘤细胞凋亡。 |
| 英文摘要: |
| Objective To investigate the changes of chemotherapeutic drugs’ sensitivity of human oral cancer after suppressor of cytokine signaling-1 (SOCS1) gene silencing.Methods Western blotting and real-time PCR were used to verify the downregulation of SOCS1 human oral cancer cell line (KB) after transfection;and the change of chemotherapeutic drugs’ sensitivity was detected by MTT assay;flow cytometry was used to detect the cell apoptosis rate.Results of RT-PCR and Western blotting showed that the expression levels of SOCS1 mRNA and protein were significantly decreased in small interfering SOCS1 (SOCS1-siRNA) transfected KB cells.After the silence of SOCS1,the median inhibitory concentration of chemotherapeutic drugs (5-fluorouracil and vincristine) for KB cells decreased significantly (P<0.05).The cell apoptosis rate of vincristine for KB cells significantly increased after SOCS1 gene silencing (P<0.05).The NF-κB and Caspase-3 protein expression levels in the experiment group dropped significantly compared with that of control group (P<0.05).Conclusions Inhibition of SOCS1 gene expression of oral cancer KB cells enhances the sensitivity to chemotherapeutic drugs,and promotes the apoptosis of cancer cells induced by chemotherapeutic drugs. |
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