Inhibition of ATM enhances the immunogenicity of triple-negative breast cancer by promoting MHC-I expression.

ABSTRACT: The immunotherapy has achieved some efficacy in triple-negative breast cancer (TNBC), but the benefit population is limited, primarily due to an abnormal immune microenvironment. Thus, it is necessary to explore new molecular targets to enhance the immunogenicity of TNBC cells and improve their responsiveness to immunotherapy. We found that a key component of the DNA repair system, Ataxia telangiectasia mutated (ATM), may function as an immune response inhibitor. In this study, the inverse correlation between ATM and CD8⁺ T cells and tumor-infiltrating lymphocytes (TILs) was confirmed by immunochemical staining of 191 TNBC specimens. Subsequently, inhibition of ATM increased the expression of major histocompatibility complex I (MHC-I) and enhanced the infiltration and cytotoxic

SUBMITTER: Li J 

PROVIDER: S-EPMC12361503 | biostudies-literature | 2025 Aug

REPOSITORIES: biostudies-literature