[1]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(原第三军医大学学报),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].J Amry Med Univ (J Third Mil Med Univ),2011,33(22):2370-2375.
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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(/HTML )
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陆军军医大学学报(原第三军医大学学报)[ISSN:1000-5404/CN:51-1095/R]

卷:
33卷
期数:
2011年第22期
页码:
2370-2375
栏目:
论著
出版日期:
2011-11-30

文章信息/Info

Title:
Emodin down-regulates ERCC1 and Rad51 and inhibits proliferation in non-small cell lung cancer cells
作者:
何林毕娟娟郭倩余音叶秀峰李伟
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
Author(s):
He Lin Bi Juanjuan Guo Qian Yu Yin Ye Xiufeng Li Wei
Chongqing Key Laboratory of Neurobiology, Department of Pathology, College of Basic Medical Sciences, Chongqing Medical University, Chongqing, 400016, China
关键词:
大黄素ERCC1Rad51U0126空泡变性
Keywords:
emodin ERCC1 Rad51 U0126 vacuolar degeneration
分类号:
R285.5;R730.23;R734.2
文献标志码:
A
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IC50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(P<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(P<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(P<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-diphenyltetrazolium 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 IC50  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 (P<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  (P<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 (P<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.

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[1]夏珊,李世荣,刘剑毅,等.大黄素对人增生性瘢痕成纤维细胞的增殖抑制及细胞内游离Ca2+的作用[J].陆军军医大学学报(原第三军医大学学报),2007,29(20):1982.
 XIA Shan,LI Shi-rong,LIU Jian-yi,et al.Effect of emodin on proliferation and intracellular free calcium of hypertrophic scar fibroblasts in vitro[J].J Amry Med Univ (J Third Mil Med Univ),2007,29(22):1982.
[2]晁荣,靳蕊蕊,陈彻,等.大黄素诱导白血病KG-1a细胞凋亡及对Bcl-2/Bax mRNA表达的影响[J].陆军军医大学学报(原第三军医大学学报),2012,34(13):1297.
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更新日期/Last Update: 2011-11-21