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全反式维甲酸和三氧化二砷抑制子宫内膜癌细胞生长及其与NDRG1基因的关系

陈玲,耿晓星   

  1. 150040 哈尔滨 哈尔滨医科大学附属第三医院妇科
  • 收稿日期:2013-01-04 修回日期:2013-03-06 出版日期:2013-05-31 发布日期:2013-05-31
  • 通讯作者: 耿晓星

The inhibitory effect of all-trans retinoic acid and arsenic trioxide on the growth of endometrial cancer cells and the relation with NDRG1

CHEN Ling, GENG Xiaoxing   

  1. Department of Gynecology,the Third Affiliated Hospital to Harbin Medical University,Harbin 150040,China
  • Received:2013-01-04 Revised:2013-03-06 Online:2013-05-31 Published:2013-05-31
  • Contact: GENG Xiaoxing

摘要: 目的 探讨全反式维甲酸(ATRA)和三氧化二砷(As2O3)对人子宫内膜癌HEC-2B细胞体外生长的抑制作用及其与分化相关基因1(NDRG1)的关系。方法 采用MTT法比较不同浓度(1×10-7、5×10-7、1×10-6、5×10-6和1×10-5mol/L)ATRA和(1.0、2.0、4.0、8.0和16.0μmol/L)As2O3对子宫内膜癌HEC-2B细胞的增殖抑制作用,Western blotting检测HEC-2B细胞中NDRG1蛋白的表达情况。结果 镜下观察,经ATRA和As2O3作用48h后的子宫内膜癌HEC-2B细胞呈现凋亡的特征性改变。1×10-7~1×10-5mol/L 的ATRA和1.0~16.0μmol/L的As2O3能够抑制子宫内膜癌HEC-2B细胞的生长,呈剂量和时间依赖性。ATRA和As2O3能够从蛋白水平调节NDRG1的表达,其表达随药物浓度的增加逐渐下调。结论 ATRA和As2O3能够抑制子宫内膜癌HEC-2B细胞的生长,该抑制作用可能与NDRG1蛋白下调有关。

Abstract: Objective To explore the inhibitory effect of all-trans retinoic acid(ATRA)and arsenic trioxide(As2O3)on the growth of human endometrial cancer HEC-2B cells in vitro and its relation with N-myc downstream regulated gene1(NDRG1)protein. Methods Tetrazolium salt assay(MTT)was used to compare the inhibitory effect of different concentration of ATRA(1×10-7,5×10-7,1×10-6,5×10-6 and 1×10-5mol/L)and As2O3(1.0, 2.0, 4.0, 8.0 and 16.0μmol/L)on the growth of HEC-2B cells. The expression of NDRG1 protein was determined by Western blotting analysis. Results After treated with ATRA and As2O3 for 48h,the HEC-2B cells showed apoptotic change. ATRA 1×10-7-1×10-5mol/L and As2O3 1.0-16.0μmol/L inhibited the cell proliferation in a dose-and time-dependent manner. Western blotting method showed that ATRA and As2O3 down-regulated the expression of NDRG1 protein in a dose-dependent manner. Conclusion ATRA and As2O3 can significantly inhibit the growth of human endometrial cancer HEC-2B cells in vitro. The effect may be related to the down-regulation of NDRG1 protein expression.

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