Cancer Genetics and Epigenetics, 2025, Vol.13, No.2, 62-76 http://medscipublisher.com/index.php/cge 66 homologous recombination function and exacerbates gene instability (Figure 1), which reflects its role in DNA repair and maintaining gene stability (Kumar et al., 2023). This means that treating the DNA repair mechanism may become an effective way to combat EAC. Figure 1 APE1 overexpression in normal esophageal cells induces DNA breaks, HR, and chromosomal or mutational instability; (B) impact on karyotype: karyotypes of control (I) and APE1O (II–III) cells examined after 60 days in culture. Panels II and III are 2 different examples of karyotypes. Mitotic index (MI) of APE1O=3.9%; 9–12 chromosome aberrations (arrowheads on representative translocations); (C) impact on mutational frequency evaluated by WGS: cells were cultured for 60 days and analyzed for new mutations, relative to baseline (day 0) cells using WGS (Adopted from Kumar et al., 2023) Figure 1 shows the important role of APE1 in esophageal adenocarcinoma (EAC). APE1 is a key enzyme in DNA repair and is of great significance for maintaining gene stability and preventing the accumulation of mutations. The figure details that when APE1 is excessive, it makes DNA more prone to breakage, enhances homologous recombination, leads to gene instability and chromosome rearrangement, and ultimately causes cancer to worsen. This discovery indicates that APE1 is not only related to the stability of the EAC gene, but also a potential therapeutic target. By regulating it, it is possible to find new strategies to inhibit the occurrence and development of tumors.
RkJQdWJsaXNoZXIy MjQ4ODYzNA==