胡黄连苷Ⅱ通过MEK/ERK通路抑制食管癌细胞增殖及侵袭转移的机制研究

杨谦; 张军; 马玉泉; 谭雪敏

doi:10.14009/j.issn.1672-2124.2021.07.012

您当前的位置：

首页 >

文章列表页 >

胡黄连苷Ⅱ通过MEK/ERK通路抑制食管癌细胞增殖及侵袭转移的机制研究

论著 | 更新时间：2022-10-08

- 胡黄连苷Ⅱ通过MEK/ERK通路抑制食管癌细胞增殖及侵袭转移的机制研究
- Mechanism of Picroside Ⅱ Inhibiting Proliferation,Invasion and Metastasis of Esophageal Cancer Cells Through MEK/ERK Pathway
- 中国医院用药评价与分析 2021年21卷第7期页码：820-825
- 作者机构：
  
  邯郸市中心医院胸外二科
- 作者简介：
- 基金信息：
- DOI：10.14009/j.issn.1672-2124.2021.07.012
  中图分类号： R285
- 纸质出版日期：2021，
扫描看全文
杨谦, 张军, 马玉泉, 等. 胡黄连苷Ⅱ通过MEK/ERK通路抑制食管癌细胞增殖及侵袭转移的机制研究[J]. 中国医院用药评价与分析, 2021,21(7):820-825.

YANG Qian, ZHANG Jun, MA Yuquan, et al. Mechanism of Picroside Ⅱ Inhibiting Proliferation,Invasion and Metastasis of Esophageal Cancer Cells Through MEK/ERK Pathway[J]. 2021,21(7):820-825.
杨谦, 张军, 马玉泉, 等. 胡黄连苷Ⅱ通过MEK/ERK通路抑制食管癌细胞增殖及侵袭转移的机制研究[J]. 中国医院用药评价与分析, 2021,21(7):820-825. DOI： 10.14009/j.issn.1672-2124.2021.07.012.

YANG Qian, ZHANG Jun, MA Yuquan, et al. Mechanism of Picroside Ⅱ Inhibiting Proliferation,Invasion and Metastasis of Esophageal Cancer Cells Through MEK/ERK Pathway[J]. 2021,21(7):820-825. DOI： 10.14009/j.issn.1672-2124.2021.07.012.

摘要

目的:探讨胡黄连苷Ⅱ通过丝裂原活化的细胞外信号调节激酶(mitogen extracellular signal regulated kinase

MEK)/细胞外信号调节激酶(extracellular signal regulated kinase

ERK)通路抑制食管癌Eca109细胞增殖及侵袭转移的作用机制。方法:将人食管癌细胞Eca109分为正常培养组(常规培养)、胡黄连苷Ⅱ组(20μmol/L胡黄连苷Ⅱ)、激活剂组(20μmol/L MEK/ERK信号通路激活剂)以及胡黄连苷Ⅱ+激活剂组(20μmol/L胡黄连苷Ⅱ培养液+20μmol/L MEK/ERK信号通路激活剂)。以四唑盐法检测四组Eca109细胞增殖活性

以流式细胞仪检测四组Eca109细胞凋亡及周期情况

以Transwell小室、划痕实验检测细胞侵袭及迁移能力

以蛋白免疫印迹法检测细胞凋亡相关蛋白、周期相关蛋白以及MEK/ERK通路相关蛋白表达情况。结果:与正常培养组相比

胡黄连苷Ⅱ组细胞增殖抑制率、细胞凋亡率

Caspase-3、Bax蛋白表达

G0/G1期、S期比例升高; Bcl-2蛋白

G2/M期比例

侵袭细胞数、划痕愈合率

细胞周期相关蛋白、MEK/ERK通路相关蛋白表达降低

上述差异均有统计学意义(P <0.05)。与正常培养组相比

激活剂组细胞增殖抑制率、细胞凋亡率

Caspase-3、Bax蛋白表达

G0/G1期、S期比例降低; Bcl-2蛋白

G2/M期比例

侵袭细胞数、划痕愈合率

细胞周期相关蛋白、MEK/ERK通路相关蛋白表达升高

上述差异均有统计学意义(P <0.05)。与胡黄连苷Ⅱ组相比

胡黄连苷Ⅱ+激活剂组细胞增殖抑制率、细胞凋亡率

Caspase-3、Bax蛋白表达

G0/G1期、S期比例降低; Bcl-2蛋白

G2/M期比例

侵袭细胞数、划痕愈合率

细胞周期相关蛋白、MEK/ERK通路相关蛋白表达升高

上述差异均有统计学意义(P <0.05)。与激活剂组相比

胡黄连苷Ⅱ+激活剂组细胞增殖抑制率、细胞凋亡率

Caspase-3、Bax蛋白表达

G0/G1期、S期比例升高; Bcl-2蛋白

G2/M期比例

侵袭细胞数、划痕愈合率

细胞周期相关蛋白、MEK/ERK通路相关蛋白表达降低

上述差异均有统计学意义(P <0.05)。结论:胡黄连苷Ⅱ对食管癌细胞的增殖及侵袭转移具有一定的抑制作用

可能通过抑制MEK/ERK通路相关蛋白的表达来发挥作用。

Abstract

OBJECTIVE: To probe into the mechanism of picroside Ⅱ inhibiting proliferation

invasion and metastasis of esophageal cancer Eca109 cells through mitogen extracellular signal regulated kinase（ MEK）/extracellular signal regulated kinase（ ERK） pathway. METHODS: Human esophageal cancer cells Eca109 were divided into normal culture group（ conventional culture）

picroside Ⅱ group（ 20 μmol/L of picroside Ⅱ）

activator group（ 20 μmol/L of MEK/ERK signaling pathway activator） and picroside Ⅱ + activator group（ 20 μmol/L of picroside Ⅱ + 20 μmol/L of MEK/ERK signaling pathway activator）. The proliferative activity of Eca109 cells in each group was detected by tetrazolium salt method

the apoptosis and cycle of Eca109 cells in each group were detected by flow cytometry

the cell invasive and metastasizing ability were detected by Transwell and scratch assay

the expression of apoptosis-related proteins

cycle-related proteins and MEK/ERK pathway-related proteins were detected by protein immunoblotting.RESULTS: Compared with the normal culture group

the inhibition rate of cell proliferation

apoptosis rate

Caspase-3 and Bax protein expression

G0/G1 phase and S phase ratio were increased in the picroside Ⅱ group; the Bcl-2 protein

G2/M phase ratio

invasion cell number

scratch healing rate

cell cycle-related proteins and MEK/ERK pathway-related proteins of picroside Ⅱ group were decreased

with statistically significant differences（ P < 0. 05）.Compared with the normal culture group

the inhibition rate of cell proliferation

apoptosis rate

Caspase-3 and Bax protein expression

G0/G1 phase and S phase ratio were decreased in the activator group; the Bcl-2 protein

G2/M phase ratio

invasion cell number

scratch healing rate

cell cycle-related proteins and MEK/ERK pathway-related proteins of the activator group were significantly increased

with statistically significant differences（ P < 0. 05）.Compared with the picroside Ⅱ group

the inhibition rate of cell proliferation

apoptosis rate

Caspase-3 and Bax protein expression

G0/G1 phase and S phase ratio were decreased in the picroside Ⅱ + activator group; the Bcl-2 protein

G2/M phase ratio

invasion cell number

scratch healing rate

cell cycle-related proteins and MEK/ERK pathway-related proteins of the picroside Ⅱ + activator group were significantly increased

with statistically significant differences（ P < 0. 05）. Compared with activator group

the inhibition rate of cell proliferation

apoptosis rate

Caspase-3 and Bax protein expression

G0/G1 phase and S phase ratio were increased in the picroside Ⅱ + activator group; the Bcl-2 protein

G2/M phase ratio

invasion cell number

scratch healing rate

cell cycle-related proteins and MEK/ERK pathway-related proteins of the picroside Ⅱ + activator group were significantly decreased

with statistically significant differences（ P < 0. 05）. CONCLUSIONS: picroside Ⅱ has a certain inhibitory effect on the proliferation

invasion and metastasis of esophageal cancer cells

probably through inhibiting the expression of MEK/ERK pathway-related proteins.

关键词

胡黄连苷ⅡMEK/ERK通路食管癌侵袭转移

Keywords

Picroside ⅡMEK/ERK pathwayEsophageal cancerInvasion and metastasis

references

查看原文

浏览量

下载量

CSCD

文章被引用时，请邮件提醒。

提交

工具集

关联资源

卡瑞利珠单抗联合白蛋白紫杉醇和顺铂一线治疗晚期食管癌的疗效及对外周血PD-1、PD-L1的影响

基于成本-效果分析的新辅助化疗联合手术与单纯手术治疗晚期食管癌的经济学评价