大黄素下调ERCC1和Rad51对非小细胞肺癌增殖的影响及分子机制

何林; 毕娟娟; 郭倩; 余音; 叶秀峰; 李伟

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大黄素下调ERCC1和Rad51对非小细胞肺癌增殖的影响及分子机制

论著 | 更新时间：2025-01-15

- 大黄素下调ERCC1和Rad51对非小细胞肺癌增殖的影响及分子机制
- Emodin down-regulates ERCC1 and Rad51 and inhibits proliferation in non-small cell lung cancer cells
- 陆军军医大学学报 2011年33卷第22期页码：2370-2375
- 作者机构：
  
  重庆医科大学基础医学院病理学教研室，重庆市神经生物学重点实验室
- 作者简介：
- 基金信息：
- DOI：
  中图分类号： R734.2;R285.5;R730.23
- 纸质出版日期：2011，
  
  网络出版日期：2011-11-30，
- 稿件说明：
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何林, 毕娟娟, 郭倩, 等. 大黄素下调ERCC1和Rad51对非小细胞肺癌增殖的影响及分子机制[J]. 陆军军医大学学报, 2011,33(22):2370-2375.

HE LIN, BI JUANJUAN, GUO QIAN, et al. Emodin down-regulates ERCC1 and Rad51 and inhibits proliferation in non-small cell lung cancer cells. [J]. Journal of army medical university, 2011, 33(22): 2370-2375.
何林, 毕娟娟, 郭倩, 等. 大黄素下调ERCC1和Rad51对非小细胞肺癌增殖的影响及分子机制[J]. 陆军军医大学学报, 2011,33(22):2370-2375. DOI：

HE LIN, BI JUANJUAN, GUO QIAN, et al. Emodin down-regulates ERCC1 and Rad51 and inhibits proliferation in non-small cell lung cancer cells. [J]. Journal of army medical university, 2011, 33(22): 2370-2375. DOI：

摘要

目的研究大黄素对非小细胞肺癌的细胞毒性，并观察其对非小细胞肺癌ERCC1和Rad51表达的影响。方法培养肺腺癌细胞株A549和肺鳞癌细胞株SK-MES-1，据MTT法测定结果将细胞分为5组：①对照组；②大黄素处理组；③溶剂处理组；④U0126处理组；⑤大黄素联合U0126处理组。细胞以不同浓度的大黄素处理48 h后分为4组。用RT-PCR和Western blot法测定目的基因RECC1和Rad51的表达情况，透射电镜观察两种细胞在大黄素作用前后的变化。结果 MTT法测定出大黄素作用48 h时A549和 SK-MES-1细胞株IC

值分别为（70.18±1.94）μmol/L和（41.95±1.27）μmol/L。大黄素100 μmol/L处理A549和SK-MES-1 48 h后抑制率为（60.42±1.37）%和（75.48±0.48）%，明显高于其他组（

0.05）。RT-PCR和Western blot检测结果显示：大黄素作用A549和SK-MES-1浓度越大，ERCC1和Rad51表达水平越低，且差异具有统计学意义（

0.05）。大黄素与ERK信号通路阻滞剂U0126联合使用时，ERCC1和Rad51表达明显低于大黄素和U0126单独使用（

0.05）。大黄素对A549和SK-MES-1细胞均具有生长抑制作用，其细胞毒性呈浓度依赖性。电镜观察可见大黄素处理的A549和SK-MES-1细胞有空泡变性。结论大黄素可降低ERCC1和Rad51的表达，从而引起非小细胞肺癌细胞生长抑制。

Abstract

Objective To study emodin-mediated cytotoxicity and determine the effect of emodin on Rad51 and ERCC1 expression in non-small cell lung cancer (NSCLC). Methods A549 cells and SK-MES-1 cells were cultured and their viability was evaluated by 3-(4

5-dimethylthiazol-2-yl)-2

5-diphenyltet

razolium bromide (MTT) assay. Then the cells were treated by emodin

menstruum

U0126 (ERK signal passway inhibitor)

or emodin+U0126 respectively. After the cells were treated with emodin at different concentrations for 48 h

the mRNA and protein levels of ERCC1 and Rad51 were determined by RT-PCR and Western blot analysis. The ultrastructure of A549 and SK-MES-1 cells were observed by transmission electron microscopy before and after emodin treatment. Results After emodin treatment for 48 h

MTT assay showed that the IC

values of A549 cells and SK-MES-1 cells were 70.18±1.94 and 41.95±1.27 μmol/L

respectively. Cell proliferation inhibition ratio in A549 and SK-MES-1 cells were (60.42±1.37)% and (75.48±0.48)% after 100 μmol/L emodin treatment for 48 h

respectively

and were significantly higher than those in cells after other treatment (

0.05). RT-PCR and Western blot analysis showed that emodin inhibited the mRNA and protein levels of ERCC1 and Rad51 in A549 and SK-MES-1 cells in a dose dependent manner (

0.05). The combination of emodin and U0126 had a stronger effect on inhibiting the expressions of Rad51 and ERCC1 when compared with single drug at the same dose (

0.05). Emodin mediated cytotoxicity in NSCLC was in a dose dependent manner. Transmission electron microscopy displayed vacuolar degenerations were observed in A549 and SK-MES-1 cells after emodin treatment. Conclusion Emodin inhibits cell proliferation in NSCLC by downregulating ERCC1 and Rad51.

关键词

大黄素ERCC1Rad51U0126空泡变性

Keywords

emodinERCC1Rad51U0126vacuolar degeneration

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