APE1 acetylation regulates autophagy induced by ionizing radiation in HeLa cells

张志敏; 杨镇洲; 何昊; 蓝保华; 李钱; 吴艳; 王帅; 李娟

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APE1 acetylation regulates autophagy induced by ionizing radiation in HeLa cells

更新时间：2026-01-09

- APE1 acetylation regulates autophagy induced by ionizing radiation in HeLa cells
- Journal of Army Medical University Vol. 38, Issue 4, Pages: 380-384(2016)
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  CLC： R341;R730.23;R737.33
- Published：2016
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张志敏,杨镇洲,何昊,蓝保华,李钱,吴艳,王帅,李娟.APE1乙酰化调节电离辐射诱导的HeLa细胞自噬[J].陆军军医大学学报(原第三军医大学学报),2016,38(04):380-384.

　Zhang Zhimin,Yang Zhenzhou,He Hao,Lan Baohua,Li Qian,Wu Yan,Wang Shuai,Li Juan.APE1 acetylation regulates autophagy induced by ionizing radiation in HeLa cells[J].J Amry Med Univ (J Third Mil Med Univ),2016,38(04):380-384.
张志敏,杨镇洲,何昊,蓝保华,李钱,吴艳,王帅,李娟.APE1乙酰化调节电离辐射诱导的HeLa细胞自噬[J].陆军军医大学学报(原第三军医大学学报),2016,38(04):380-384. DOI：

　Zhang Zhimin,Yang Zhenzhou,He Hao,Lan Baohua,Li Qian,Wu Yan,Wang Shuai,Li Juan.APE1 acetylation regulates autophagy induced by ionizing radiation in HeLa cells[J].J Amry Med Univ (J Third Mil Med Univ),2016,38(04):380-384. DOI：

摘要

目的探讨脱嘌呤/脱嘧啶核酸内切酶∕氧化还原因子(apurinic/aprimidinic endonuclease/redox factor-1，APE1/Ref-1)乙酰化对电离辐射诱导HeLa细胞自噬的调节作用。方法给予Elekta precise直线加速器处理HeLa细胞及子系细胞APE1

和APE1

K6R/K7R

，应用免疫共沉淀(co-immunoprecipitation，Co-IP)的方法检测APE1乙酰化修饰及Beclin1/Bcl2的结合，流式细胞仪检测细胞自噬的水平，免疫荧光激光共聚焦检测LC3的聚集，Western blot检测APE1、LC3和p62的表达。结果 HeLa细胞APE1乙酰化水平随着照射剂量的增加和照射后时间的延长而逐渐升高(P0.05)。HeLa细胞 LC3Ⅱ的表达与照射剂量呈正相关，而与p62呈负相关(P0.05)；电离辐射促进细胞的自噬水平和LC3的聚集。电离辐射后，LC3Ⅱ上调；与对照组APE1

相比，APE1

K6R/K7R

细胞Beclin1/Bcl2结合增强，LC3Ⅱ/LC3Ⅰ比值降低，p62表达上调(P0.05)。结论 APE1乙酰化通过Beclin1/Bcl2途径调节电离辐射诱导的HeLa细胞自噬。

Abstract

Objective To explore the relationship between apurinic/aprimidinic endonuclease/redox factor-1 (APE1) acetylation and autophagy induced by ionizing radiation in HeLa cells. Methods HeLa cells

APE1

K6R/K7R

cells and APE1

cells underwent radiation treatment with Elekta precise linear accelerator

and APE1 acetylation and interaction of Beclin1 and Bcl2 were detected by co-immunoprecipitation (Co-IP). Flow cytometry was used to analyze HeLa cell autophag

y level

LC3 accumulation was observed by immunofluorescence assay

and Western blotting was adopted to measure the expression of APE1

LC3 and p62. Results The APE1 acetylation was increased along with the increase of the radiation dose and the time after radiation in HeLa cells

and the increase of APE1 acetylation was in a time- and dose-dependent manner (P0.05). LC3Ⅱ expression was positively correlated with the radiation dose in HeLa cells

while p62 expression was opposite (P0.05). LC3 accumulation and autophagy increased after ionizing radiation

and the LC3Ⅱ expression was up-regulated (P0.05). Compared with APE1

cells

the interaction of Beclin1 and Bcl2 was enhanced in APE1

K6R/K7R

cells

LC3Ⅱ/LC3Ⅰ ratio was decreased

and p62 expression was up-regulated after ionizing radiation (P0.05). Conclusion APE1 acetylation is increased after ionizing radiation

which can promote radiation-induced autophagy via Beclin1/Bcl2 pathway in HeLa cells.

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张志敏

杨镇洲

何昊

蓝保华

李钱

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王帅

李娟

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