Role of PPARγ activation in cell growth inhibition and apoptosis inducement by ampelopsin in breast cancer cells

Yong ZHOU; Jinying ZHENG; Xiaoling JIN; Xiaohua XU; Li RAN; Qianyong ZHANG; Jundong ZHU; Mantian MI

doi:10.16016/j.1000-5404.201712210

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Role of PPARγ activation in cell growth inhibition and apoptosis inducement by ampelopsin in breast cancer cells

Basic Medicine | 更新时间：2026-01-09

- Role of PPARγ activation in cell growth inhibition and apoptosis inducement by ampelopsin in breast cancer cells
- Journal of Third Military Medical University Vol. 40, Issue 13, Pages: 1185-1191(2018)
- 作者机构：
  
  1.401320 重庆，重庆市巴南区人民医院临床营养科
  2.400038 重庆，陆军军医大学(第三军医大学)军事预防医学系营养与食品卫生学教研室
- 作者简介：
- 基金信息：
  
  the Project of Basic Science and Frontier Technology Research of Chongqing(CSTC2017jcyjAX0305);the Open Project of Key Laboratory of Electromagnetic Radiation Medical Protection of Ministry of Education, Army Medical University(2017DCKF002)
- DOI：10.16016/j.1000-5404.201712210
  CLC： R151.3;R730.23;R737.9
- Received：22 December 2017，
  
  Revised：2018-01-25，
  
  Published：15 July 2018
- 稿件说明：
移动端阅览
Yong ZHOU, Jinying ZHENG, Xiaoling JIN, et al. Role of PPARγ activation in cell growth inhibition and apoptosis inducement by ampelopsin in breast cancer cells[J]. Journal of Third Military Medical University, 2018, 40(13): 1185-1191.
DOI：

Yong ZHOU, Jinying ZHENG, Xiaoling JIN, et al. Role of PPARγ activation in cell growth inhibition and apoptosis inducement by ampelopsin in breast cancer cells[J]. Journal of Third Military Medical University, 2018, 40(13): 1185-1191. DOI： 10.16016/j.1000-5404.201712210.

摘要

目的

探讨过氧化物酶体增殖激活物受体γ(peroxisome proliferators-activated receptorγ

PPARγ)的激活在蛇葡萄素(ampelopsin

AMP)抑制乳腺癌细胞增殖和诱导细胞增殖凋亡中的作用。

方法

以不同浓度AMP(20、40、60、80 μmol/L)分别处理人乳腺癌MDA-MB-231、MCF-7细胞24 h后，荧光素酶报告基因法检测AMP对PPARγ的激活作用，CCK-8检测细胞活力，流式细胞仪检测细胞凋亡，Western blot检测凋亡相关蛋白的表达，Caspase-3活性检测试剂盒检测Caspase-3活性。

结果

与PPARγ激动剂罗格列酮一样，AMP剂量依赖性地增强报告基因荧光素酶活性，同时显著抑制乳腺癌细胞增殖并诱导细胞凋亡(

＜0.05)；Western blot检测结果显示，AMP在显著上调乳腺癌细胞凋亡相关蛋白Bax、PTEN、活化Caspase-3表达的同时下调Bcl-2蛋白及Bcl-2/Bax比值；激酶活性检测结果显示，AMP可显著增强Caspase-3激酶活性，以上作用均可被PPARγ特异性拮抗剂GW9662显著削弱。

结论

AMP可能是PPARγ的天然激动剂，其通过激活PPARγ信号途径抑制乳腺癌细胞增殖并诱导细胞凋亡。

Abstract

Objective

To investigate whether the activation of proliferators-activated receptor γ (PPARγ) is required for ampelopsin (AMP)-induced cell growth inhibition and apoptosis in human breast cancer cells.

Methods

After different concentrations of AMP (20

60 and 80 μmol/L) was used to treat breast cancer cell lines MCF-7 and MDA-MB-231 for 24 h respectively

PPARγ activity was measured by luciferase reporter assay

cell viability was assessed by CCK-8 assay

and cell apoptosis was measured by flow cytometry with Annexin V-FITC/PI staining. Western blotting was used to measure the expression of apoptosis related proteins

and a clorimetric assay kit was employed to detect Caspase-3 activity.

Results

As PPARγ agonist rosiglitazone

AMP treatment also enhanced the activity of luciferase rep

orter

inhibited cell viability and induced apoptosis (

0.05) in MCF-7 and MDA-MB-231 cells in dose-dependent manners. Furthermore

Western blotting showed that AMP significantly up-regulated apoptosis related proteins Bax and PTEN

activated Caspase-3

down-regulated Bcl-2 and decreased the ratio of Bcl-2/Bax. Clorimetric assay indicated that the treatment enhanced the activity of Caspase-3. All above results could be obviously attenuated by PPARγ specific antagonist GW9662.

Conclusion

AMP maybe a natural agonist of PPARγ

and it can suppress cell proliferation and induce apoptosis in breast cancer cells by activating PPARγ.

关键词

Keywords

references

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