AG490对食管鳞癌Eca-109细胞增殖、凋亡及放疗敏感性的影响

臧春宝; 万跃; 王勇; 侯妍利; 唐敏; 李少林

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AG490对食管鳞癌Eca-109细胞增殖、凋亡及放疗敏感性的影响

论著 | 更新时间：2026-01-09

- AG490对食管鳞癌Eca-109细胞增殖、凋亡及放疗敏感性的影响
- Effect of Janus kinase inhibitor AG490 on proliferation, apoptosis and radiosensitivity of human esophageal carcinoma Eca-109 cells
- 陆军军医大学学报 2013年35卷第13期页码：1357-1361
- 作者机构：
- 作者简介：
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  中图分类号： R73-36;R735.1;R977.3
- 纸质出版：2013
- 稿件说明：
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臧春宝,万跃,王勇,侯妍利,唐敏,李少林.AG490对食管鳞癌Eca-109细胞增殖、凋亡及放疗敏感性的影响[J].陆军军医大学学报(原第三军医大学学报),2013,35(13):1357-1361.

　Zang Chunbao,Wan Yue,Wang Yong,Hou Yanli,Tang Min,Li Shaolin.Effect of Janus kinase inhibitor AG490 on proliferation, apoptosis and radiosensitivity of human esophageal carcinoma Eca-109 cells[J].J Amry Med Univ (J Third Mil Med Univ),2013,35(13):1357-1361.
臧春宝,万跃,王勇,侯妍利,唐敏,李少林.AG490对食管鳞癌Eca-109细胞增殖、凋亡及放疗敏感性的影响[J].陆军军医大学学报(原第三军医大学学报),2013,35(13):1357-1361. DOI：

　Zang Chunbao,Wan Yue,Wang Yong,Hou Yanli,Tang Min,Li Shaolin.Effect of Janus kinase inhibitor AG490 on proliferation, apoptosis and radiosensitivity of human esophageal carcinoma Eca-109 cells[J].J Amry Med Univ (J Third Mil Med Univ),2013,35(13):1357-1361. DOI：

摘要

目的研究Janus激酶抑制剂AG490对食管鳞癌Eca-109细胞增殖、凋亡及放疗敏感性的影响，并探讨其作用机制。方法用不同浓度(0、25、50、100 μmol/L)的AG490处理Eca-109细胞，采用MTT法检测细胞增殖，Annexin V-FITC/PI双染流式细胞仪检测细胞凋亡，克隆形成实验检测细胞放疗敏感性，Western blot 检测各组细胞Stat3、p-Stat3、Bcl-2、Bax蛋白表达。结果与对照组比较，AG490各浓度组(25、50、100 μmol/L)在AG490作用后第1~5天Eca-109细胞增殖减慢，呈量效-时效关系(

0.05

0.01)。与对照组比较，AG490各浓度组(25、50、100 μmol/L)在AG490作用48 h后Eca-109细胞凋亡率增加，呈量效关系(

0.01)。与对照组比较，各剂量X射线照射后50 μmol/L组细胞存活率降低，放射生物学参数SF

、D

、N值均降低(

0.05)，SERD

和SERD

值增加(

0.05)。与对照组比较，AG490 50 μmol/L+4Gy组和AG490 50 μmol/L组p-Stat3蛋白表达下调(

0.05

0.01)。与对照组比较，AG490各浓度(50和100 μmol/L)组Bcl-2的表达降低(

0.05)、Bax的表达增加(

0.05)。结论 AG490抑制Eca-109细胞增殖，增加细胞凋亡，增加放疗敏感性，其机制可能是通过阻断Stat3蛋白的活化，调控凋亡蛋白（Bcl-2和Bax）的表达。

Abstract

Objective To investigate the effect and mechanism of Janus kinase inhibitor AG490 on the proliferation

apoptosis and radiosensitivity of human esophageal carcinoma Eca-109 cells. Methods Eca-109 cells were tr

eated with different concentrations of AG490 (0

50 and 100 μmol/L). Cell proliferation and apoptosis were detected by MTT assay and flow cytometry

respectively

and cell radiosensitivity was measured by colony formation assay. The expression levels of Stat3

p-Stat3

Bcl-2 and Bax were evaluated by Western blotting. Results Compared with the control group (0 μmol/L)

the proliferation of Eca-109 cells in AG490 treatment groups (25

50 and 100 μmol/L) significantly decreased at 1-5 d after treatment in a dose- and time-dependent manner (

0.05

0.01). Compared with the control group (0 μmol/L)

the apoptosis of Eca-109 cells in AG490 treatment groups (25

50 and 100 μmol/L) significantly increased at 48 h after treatment in a dose-dependent manner (

0.01). Compared with the control group (0 μmol/L)

the cell survival fraction and radiobiological parameters (SF

and N) of the AG490 50 μmol/L group significantly decreased (

0.05)

and the sensitivity enhancement ratio (SERD

and SERD

) significantly increased (

0.05). Compared with the control group (0 μmol/L)

the expression of p-Stat3 in AG490 50 μmol/L+4 Gy group and AG490 50 μmol/L group significantly decreased (

0.05

0.01). Compared with the control group (0 μmol/L)

the expression of Bcl-2 in AG490 treatment groups (50 and 100 μmol/L) significantly decreased (

0.05)

and the expression of Bax significantly increased (

0.05). Conclusion AG490 can regulate the expression of Bcl-2 and Bax by blocking the activation of Stat3

thus inhibiting the proliferation and increasing the apoptosis and radiosensitivity of human esophageal carcinoma Eca-109 cells in vitro.

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