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

WT

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

WT

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.