[1]李维东,罗浩军,李振华,等.雌激素激活GPER-EGFR-ERK通路促进人乳腺癌SKBR-3细胞系增殖[J].第三军医大学学报,2012,34(22):2283-2287.
 Li Weidong,Luo Haojun,Li Zhenhua,et al.Estrogen activates GPER-EGFR-ERK pathway to promote the proliferation of human breast cancer cell line SKBR-3[J].J Third Mil Med Univ,2012,34(22):2283-2287.
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《第三军医大学学报》[ISSN:1000-5404/CN:51-1095/R]

卷:
34卷
期数:
2012年第22期
页码:
2283-2287
栏目:
论著
出版日期:
2012-11-30

文章信息/Info

Title:
Estrogen activates GPER-EGFR-ERK pathway to promote the proliferation of human breast cancer cell line SKBR-3
作者:
李维东罗浩军李振华余腾华杨光伦涂刚
重庆医科大学附属第一医院内分泌乳腺外科
Author(s):
Li Weidong Luo Haojun Li Zhenhua Yu Tenghua Yang Guanglun Tu Gang
Department of Endocrine Breast Surgery, First Affiliated Hospital, Chongqing Medical University, Chongqing, 400016, China
关键词:
雌激素GPER SKBR-3增殖
Keywords:
estrogen GPER SKBR-3 proliferation
分类号:
R730.23;R737.9;R977.12
文献标志码:
A
摘要:
目的      探讨G蛋白偶联雌激素受体(G protein-coupled estrogen receptor,GPER)介导雌激素对人乳癌细胞系SKBR-3增殖的影响。      方法      激光共聚焦显微镜扫描检测钙离子探针标记的细胞内钙离子浓度随时间的变化,CCK-8法观测细胞的增殖生长,流式细胞术检测细胞周期,Western blot 检测磷酸化细胞外信号调节激酶(phospho-extracellular  regulate kinase,p-ERK)的相对表达量。      结果      17-β雌二醇(E2)与GPER激动剂(G1)(E2、G1处理组)刺激SKBR-3细胞后,细胞内钙离子浓度从120 s开始迅速升高,细胞增殖与对照组相比显著增加,CCK-8测定的(E2、G1处理组)相对细胞数分别是对照组的(2.08±0.07)倍和(2.00±0.04)倍;流式细胞术检测E2、G1处理组细胞增殖指数(PI)(E2、G1处理组)为(43.12±0.38)%、(42.43±0.52)%,较对照组(29.19±0.29)%明显增加(P<0.05);Western blot 检测结果显示E2处理组p-ERK表达量显著高于对照组(P<0.05)。GPER特异性抑制剂G15、EGFR拮抗剂AG1478、ERK拮抗剂U0126均可抑制E2、G1触发的相应变化,PI3K拮抗剂WM则不能。      结论      雌激素激活GPER-EGFR-ERK通路促进人乳腺癌SKBR-3细胞系增殖。
Abstract:
Objective      To explore the effect of estrogen on the proliferation of human breast cancer cell line SKBR-3 mediated by G protein-coupled estrogen receptor (GPER).       Methods      Calcium influx, cell growth ability and cell cycle were examined by confocal laser scanning microscopy, CCK-8 assay and flow cytometry in the presence of different concentrations of drugs, respectively. The relative expression level of phospho-extracellular signal-regulated kinase (p-ERK) was detected by Western blotting.       Results      After the cells were treated with 17-β estradiol (E2) or GFER specific agonist (G1), intracellular calcium ion concentration shifted quickly from 120 seconds, and cell proliferation increased significantly with the relative cell numbers (2.08±0.07) times and (2.0±0.04) times more than those of the control group. The proliferation index (PI) (43.12±0.38)% and (42.43±0.52)% at S phase and G2-M phase increased significantly as compared to the control group (29.19±0.29)% (P<0.05). The protein level of p-ERK was higher in the treatment group than in the control group (P<0.05). GFPE antagonist G15, EGFR antagonist AG1478 and ERK antagonist U0126 rather than PI3K antagonist wortmannin could inhibit the changes induced by E2 or G1.       Conclusion      Estrogen activates GPER-EGFR-ERK pathway to promote the proliferation of human breast cancer cell line SKBR-3.

参考文献/References:

李维东, 罗浩军, 李振华, 等. 雌激素激活GPER-EGFR-ERK通路促进人乳腺癌SKBR-3细胞系增殖[J]. 第三军医大学学报,2012,34(22):2283-2287.

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更新日期/Last Update: 2012-11-20