[1]倪振洪,王滨,丁雯,等.左旋棉酚通过ERK通路诱导Daudi细胞发生自噬及意义[J].陆军军医大学学报(原第三军医大学学报),2012,34(23):2384-2387.
　Ni Zhenhong,Wang Bin,Ding Wen,et al.(-)-gossypol induces autophagy in Daudi cells through ERK signal pathway[J].J Amry Med Univ (J Third Mil Med Univ),2012,34(23):2384-2387.
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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:
34卷
期数:
2012年第23期
页码:
2384-2387
栏目:
论著
出版日期:
2012-12-15

文章信息/Info

Title:
(-)-gossypol induces autophagy in Daudi cells through ERK signal pathway
作者:
倪振洪; 王滨; 丁雯; 程攀科; 连继勤; 何凤田
第三军医大学基础医学部生物化学与分子生物学教研室
Author(s):
Ni Zhenhong;  Wang Bin;  Ding Wen;  Cheng Panke;  Lian Jiqin;  He Fengtian
Department of Biochemistry and Molecular Biology, College of Basic Medical Sciences, Third Military Medical University, Chongqing, 400038, China
关键词:
左旋棉酚; Burkitt淋巴瘤; 细胞增殖; 自噬; ERK
Keywords:
(-)-gossypol;  Burkitt lymphoma;  cell proliferation;  autophagy
分类号:
R733.4; R965; R979.19
文献标志码:
A
摘要:
目的      探讨左旋棉酚诱导淋巴瘤Daudi细胞发生自噬可能机制及对细胞存活率的影响。      方法       采用CCK-8法检测左旋棉酚在体外对Daudi细胞增殖抑制作用的影响；采用台盼蓝排斥实验检测不同处理对细胞存活率的影响；Western blot检测细胞中自噬相关蛋白LC3、ERK和磷酸化ERK的表达情况；AO染色观察经左旋棉酚处理后Daudi细胞酸性小体的变化情况。      结果       左旋棉酚能剂量依赖性地抑制Daudi细胞的增殖和促进细胞死亡；AO染色后经左旋棉酚处理的细胞内可观察到大量的酸性小体形成；Western blot显示左旋棉酚能显著上调自噬相关蛋白LC3Ⅱ的表达及增强磷酸化ERK的水平，抑制ERK的磷酸化能下调LC3 Ⅱ的表达；ERK抑制剂U0126及自噬抑制剂CQ和3-MA均能显著增强左旋棉酚的杀细胞效力。      结论      左旋棉酚可能通过ERK通路诱导Daudi细胞发生自噬，抑制ERK介导的自噬能够显著增强左旋棉酚的抗瘤效应。
Abstract:
Objective       To investigate the mechanism of (-)-gossypol-induced autophagy and its effect on cell viability in Burkitt lymphoma Daudi cells.       Methods        CCK-8 detection was used to assess the inhibitory effects of (-)-gossypol on the proliferation in Daudi cells. Trypan blue exclusion assay was used to detect cell viability during different treatments. Western blotting was used to determine the expression of LC3 Ⅱ and ERK. Acridine orange staining was used to detect the formation of acidic vesicular organelles (AVO).       Results       (-)-gossypol inhibited cell proliferation and induced cell death in a dose-dependent manner. Increased AVOs were noted after treatment of cells with (-)-gossypol. Western blot analysis revealed that (-)-gossypol treatment markedly upregulated LC3 Ⅱ and induced phosphorylation of ERK. Inhibition of ERK activity blocked the upregulation of LC3 Ⅱ mediated by (-)-gossypol. Inhibition of autophagy by U0126 (ERK inhibitor), CQ and 3-MA (autophagy inhibitors) enhanced cell death mediated by (-)-gossypol.       Conclusion        (-)-gossypol effectively inhibits cell proliferation and induces autophagy in Burkitt lymphoma Daudi cells via ERK pathway.

相似文献/References:

[1]丁雯,倪振洪,程攀科,等.左旋棉酚通过细胞自噬下调Namalwa细胞中B淋巴细胞刺激因子的表达[J].陆军军医大学学报(原第三军医大学学报),2012,34(16):1613.
　Ding Wen,Ni Zhenhong,Cheng Panke,et al.Mechanism of (-)-gossypol down-regulating B lymphocyte stimulator expression in Namalwa cells via autophagy[J].J Amry Med Univ (J Third Mil Med Univ),2012,34(23):1613.
[2]王滨,倪振洪,丁雯,等.NVP-BEZ235增敏左旋棉酚杀伤肝癌HepG2细胞的作用[J].陆军军医大学学报(原第三军医大学学报),2013,35(19):2024.
　Wang Bin,Ni Zhenhong,Ding Wen,et al.Effect of NVP-BEZ235 on sensitization of HepG2 cells to (-)-gossypol[J].J Amry Med Univ (J Third Mil Med Univ),2013,35(23):2024.

更新日期/Last Update: 2012-12-04