TSA可能通过抑制APE1 BER功能增强顺铂的肺腺癌细胞毒性

张志敏; 杨镇洲

您当前的位置：

首页 >

文章列表页 >

TSA可能通过抑制APE1 BER功能增强顺铂的肺腺癌细胞毒性

基础医学 | 更新时间：2026-01-09

- TSA可能通过抑制APE1 BER功能增强顺铂的肺腺癌细胞毒性
- Trichostatin A enhances cisplatin-induced cytotoxicity through inhibiting base excision repair of AP endonuclease in lung adenocarcinoma cells
- 陆军军医大学学报 2017年39卷第5期页码：413-416
- 作者机构：
- 作者简介：
- 基金信息：
- DOI：
  中图分类号： R73-361;R734.2;R979.1
- 纸质出版：2017
- 稿件说明：
移动端阅览
张志敏,杨镇洲.TSA可能通过抑制APE1 BER功能增强顺铂的肺腺癌细胞毒性[J].陆军军医大学学报(原第三军医大学学报),2017,39(05 ):413-416.　Zhang Zhimin,Yang Zhenzhou.Trichostatin A enhances cisplatin-induced cytotoxicity through inhibiting base excision repair of AP endonuclease in lung adenocarcinoma cells[J].J Amry Med Univ (J Third Mil Med Univ),2017,39(05 ):413-416.

张志敏, 杨镇洲. Trichostatin A enhances cisplatin-induced cytotoxicity through inhibiting base excision repair of AP endonuclease in lung adenocarcinoma cells[J]. Journal of Army Medical University, 2017, 39(5): 413-416.
张志敏,杨镇洲.TSA可能通过抑制APE1 BER功能增强顺铂的肺腺癌细胞毒性[J].陆军军医大学学报(原第三军医大学学报),2017,39(05 ):413-416.　Zhang Zhimin,Yang Zhenzhou.Trichostatin A enhances cisplatin-induced cytotoxicity through inhibiting base excision repair of AP endonuclease in lung adenocarcinoma cells[J].J Amry Med Univ (J Third Mil Med Univ),2017,39(05 ):413-416. DOI：

张志敏, 杨镇洲. Trichostatin A enhances cisplatin-induced cytotoxicity through inhibiting base excision repair of AP endonuclease in lung adenocarcinoma cells[J]. Journal of Army Medical University, 2017, 39(5): 413-416. DOI：

摘要

目的探讨曲古抑菌素A(trichostatin A，TSA)对顺铂诱导的细胞毒性的影响。方法给予0、250、500 nmol/L TSA预处理A549细胞24 h后，分别联合0、5、10、15 μmol/L顺铂处理A549细胞24 h后，通过0、0.5、1、2 μmol/L APE1 InhibitorⅢ调控APE1 BER功能，应用CCK-8方法检测细胞增殖率，AP内切酶活性实验检测APE1 BER功能，通过流式细胞仪检测细胞凋亡水平，immunoblot检测γ-H2AX表达水平。结果 TSA联合顺铂处理A549细胞明显增强顺铂的细胞增殖抑制，并促进顺铂诱导的细胞凋亡；随着TSA浓度的升高APE1内切酶活性逐渐减弱，TSA联合顺铂促进顺铂诱导的γ-H2AX表达；利用inhibitor Ⅲ抑制APE1内切酶活性，促进顺铂诱导细胞增殖抑制和凋亡水平。结论 TSA可能通过抑制APE1BER功能增强顺铂诱导的细胞毒性反应。

Abstract

Objective To determine the effect of trichostatin A (TSA) on the cytotoxicity induced by cisplatin in lung adenocarcinoma A549 cells. Methods After the A549 cells were pretreated with TSA at 0

250 and 500 nmol/L for 24 h

the cells were treated by cisplatin at 0

10 and 15 μmol/L for another 24 h. CCK-8 assay and flow cytometry were used to detect cell proliferation and apoptosis respectively. The effect of AP endonuclease (APE1) Inhibitor Ⅲ (0

0.5

1 and 2 μmol/L) was determined by AP endonuclease activity assay for the activity of base excision repair (BER). The expression of γ-H2AX was measured by immunoblotting. Results TSA enhances the inhibitory effect of cisplatin on cell proliferation and its promoting effect on cell apoptosis. With the increased of TSA dose

the BER activity of APE1 was gradually decreased. TSA also improved the expression of γ-H2AX induced by cisplatin. APE1 inhibitor Ⅲ suppressed the activity of endonuclease

and enhanced the cell proliferation and apoptosis induced by cisplatin. Conclusion TSA enhances cytotoxicity response caused by cisplatin through inhibiting the BER activity of APE1.

关键词

Keywords

references

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

氨磷汀通过上调PKM2表达增强肾近端小管上皮细胞抵抗顺铂毒性

TAS102选择性抑制ATRX缺失胶质瘤细胞的实验研究

心肌特异性Hdac3基因缺失引起小鼠心室重构

苦参素与顺铂合用对人肝癌裸鼠皮下移植瘤组织VEGF、CD31表达的影响和意义

O-6-甲基鸟嘌呤-DNA甲基转移酶在顺铂激活的胃癌细胞自噬中的作用