ATRX loss inhibits DDR to strengthen radio-sensitization in p53-deficent HCT116 cells.

ABSTRACT: Identifying novel targets for molecular radiosensitization is critical for improving the efficacy of colorectal cancer (CRC) radiotherapy. Alpha-thalassemia/mental retardation X-linked (ATRX), a member of the SWI/SNF-like chromatin remodeling protein family, functions in the maintenance of genomic integrity and the regulation of apoptosis and senescence. However, whether ATRX is directly involved in the radiosensitivity of CRC remains unclear. Our results showed that silencing ATRX increased the radiosensitivity of HCT116 CRC cells, which was further strengthened when p53 was depleted. To explore the potential mechanism, we focused on the impact of the ionizing radiation (IR)-induced DNA damage response (DDR), apoptosis, and senescence and the activation of the Daxx/MDM2/p53 pathway caused

SUBMITTER: Qin L 

PROVIDER: S-EPMC11700193 | biostudies-literature | 2025 Jan

REPOSITORIES: biostudies-literature