Aspirin-induced acetylation of APE1/Ref-1 enhances RAGE binding and promotes apoptosis in ovarian cancer cells

• DOI: 10.4196/kjpp.24.273
• Publication Date: 2025-03-07T06:09:35Z
• Authors: Hao Jin; Yu Ran Lee; Sungmin Kim; Eun-Ok Lee; Hee Kyoung Joo; Heon Jong Yoo; Cuk-Seong Kim; Byeong Hwa Jeon
• Keywords: RAGE

The role of acetylated apurinic/apyrimidinic endonuclease 1/redox factor 1 (APE1/Ref-1) in ovarian cancer remains poorly understood. Therefore, this study aimed to investigate the combined effect recombinant human APE1/Ref-1 (rhAPE1/Ref-1) and aspirin (ASA) on two cells, PEO-14, CAOV3. viability apoptosis cells treated with rhAPE1/Ref-1 or ASA were assessed. Our results demonstrated that induced acetylation widespread hyperacetylation PEO-14 cells. Additionally, co-treatment substantially reduced cell apoptosis, not CAOV3, a dose-dependent manner. increased expression membrane localization receptor for advanced glycation endproducts (RAGEs). Acetylated showed enhanced binding RAGEs. In contrast, RAGE knockdown death poly(ADP-ribose) polymerase cleavage caused by combination treatment, highlighting importance APE1/Ref-1-RAGE interaction triggering apoptosis. Moreover, treatment effectively 3D spheroid cultures model better mimics tumor microenvironment. These demonstrate its is potential therapeutic target cancer. Thus, may offer promising new strategy inducing death.