G-protein coupled receptor improves 17β-Estradiol induced proliferation of human anaplastic thyroid carcinoma FRO cells

吴婷婷; 龙方懿; 贾朝莉; 刘智敏

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G-protein coupled receptor improves 17β-Estradiol induced proliferation of human anaplastic thyroid carcinoma FRO cells

更新时间：2026-01-09

- G-protein coupled receptor improves 17β-Estradiol induced proliferation of human anaplastic thyroid carcinoma FRO cells
- Journal of Army Medical University Vol. 33, Issue 2, Pages: 164-168(2011)
- 作者机构：
- 作者简介：
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- DOI：
  CLC： R730.23;R736.1;R977.12
- Published：2011
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吴婷婷,龙方懿,贾朝莉,刘智敏.G蛋白偶联受体在雌激素诱导人甲状腺未分化癌FRO细胞增殖中的作用及其机制[J].陆军军医大学学报(原第三军医大学学报),2011,33(02):164-168.

　Wu Tingting,Long Fangyi,Jia Chaoli,Liu Zhimin.G-protein coupled receptor improves 17β-Estradiol induced proliferation of human anaplastic thyroid carcinoma FRO cells[J].J Amry Med Univ (J Third Mil Med Univ),2011,33(02):164-168.
吴婷婷,龙方懿,贾朝莉,刘智敏.G蛋白偶联受体在雌激素诱导人甲状腺未分化癌FRO细胞增殖中的作用及其机制[J].陆军军医大学学报(原第三军医大学学报),2011,33(02):164-168. DOI：

　Wu Tingting,Long Fangyi,Jia Chaoli,Liu Zhimin.G-protein coupled receptor improves 17β-Estradiol induced proliferation of human anaplastic thyroid carcinoma FRO cells[J].J Amry Med Univ (J Third Mil Med Univ),2011,33(02):164-168. DOI：

摘要

目的探讨G蛋白偶联受体（G-protein coupled receptor，GPER）在雌激素促进人甲状腺未分化癌FRO细胞增殖中的作用及其机制。方法不同浓度（0、10

-10

、10

-9

、10

-8

mol/L）的17β-雌二醇（17β-Estradiol，E2）处理FRO细胞不同时间（0、12、24 h），MTT法检测细胞增殖率；10

-8

mol/L的E2处理FRO细胞不同时间（0～24 h），流式细胞术检测E2对FRO细胞周期的影响；设计合成针对GPER的小干扰RNA（GPER-siRNA）并转染FRO细胞；Western blot检测FRO细胞中Akt与ERK1/2磷酸化水平与GPER蛋白的表达。结果不同浓度（0、10

-10

、10

-9

、10

-8

mol/L）的E2处理FRO细胞不同时间（0、12、24 h），细胞增殖率随浓度和时间的增加而增加，且10

-8

mol/L的E2处理24 h后，细胞增殖率为（16.5±2.1）%；10

-8

mol/L的E2处理FRO细胞不同时间（0、12、24 h），细胞周期S/G

/M期细胞的比例随时间的增加而增加；E2（10

-8

mol/L）处理FRO细胞不同时间（0、5、10、15、30 min），ERK1/2与Akt的磷酸化水平分别在15 min与10 min达到最大；将GPER-siRNA转染FRO细胞48 h，GPER的蛋白表达显著减少； E2作用于分别加入PD98059（30 μmol/L）、LY294002（50 μmol/L）以及转染GPER-siRNA的FRO细胞15 min和10 min，与E2处理组相比，ERK1/2和Akt的磷酸化水平降低； E2作用于分别加入PD98059、LY294002及转染GPER-siRNA的FRO细胞24 h，与E2处理组相比，增殖率由（16.5±2.1）%降至（11.2±1.3）%、（9.6±1.5）%、（7.2±1.3）%（P0.05）。结论 E2通过GPER激活ERK1/2、PI3K-Akt途径，促进FRO细胞的增殖。

Abstract

Objective To investigate the

effect of G-protein coupled receptor (GPER) on 17β-Estradiol (E2) induced proliferation of human anaplastic thyroid carcinoma FRO cells. Methods FRO cells were treated with different concentration (0，10

-10

，10

-9

and 10

-8

mol/L) of E2 for different time periods (0，12 and 24 h)

and cell growth was evaluated by MTT assay. After the cells were treated by 10

-8

mol/L E2 for different time periods (0

12 and 24 h)

cell cycle was analyzed by flow cytometry. RNA interference against GPER (GPER-RNAi) was designed and synthesized

then transfected to FRO cells. The levels of phosphorylated ERK1/2

phosphorylated Akt and GPER were analyzed by Western blot analysis. Results Treatment with different concentration (0

-10

-9

and 10

-8

mol/L) of E2 for different times (0

12 and 24 h)

the cell growth rates were increased in dose- and time-dependent manners. When FRO cells were treated with 10

-8

mol/L E2 for 24 h

the cell growth rate was (16.5±2.1) %. After the cells were treated with 10

-8

mol/L E2 for different times (0

12 and 24 h)

the percentages of S/G

/M phase were increased in a time-dependent manner. E2-induced accumulation of phosphorylated ERK1/2 and phosphorylated Akt in FRO cells reached peak at 15 min and 10 min respectively after E2 treatment. The expression of GPER was reduced significantly when GPER-siRNA was transfected to FRO cells for 48 h. Pretreatment with PD98059 (30 μmol/L)

LY294002 (50 μmol/L) and GPER-siRNA obliterated the inductive effects of E2 on ERK1/2 phosphorylation and Akt phosphorylation at 15 min and 10 min respectively in FRO cells. Meanwhile pretreatment with PD98059

LY294002 and GPER-siRNA obliterated the inductive effects of E2 on cell growth. and the growth rates were reduced to (11.2±1.3)%

(9.6±1.5)% and (7.2±1.3)% respectively compared with those of E2-treated cells [(16.5±2.1)%

P0.05

]

. Conclusion E2 can promote proliferation of FRO cells via ERK1/2 and PI3K-A

kt pathway in a GPER-dependent manner.

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