Inhibiting ADAR1-Mediated Excessive Epigenetic A-to-I RNA Editing Improves the Immune Microenvironment and Increases Sensitivity to Immunotherapy in Lung Adenocarcinoma.

ABSTRACT: Adenosine-to-inosine (A-to-I) RNA editing, predominantly catalyzed by the enzyme adenosine deaminase acting on RNA 1 (ADAR1), has attracted interest due to its essential functions in regulating immune response and cancer progression. This research investigates ADAR1 inhibition as a promising strategy aimed at improving immunotherapy efficacy in lung adenocarcinoma (LUAD) and explores the underlying mechanisms. Findings from murine models demonstrate that ADAR1 suppression within tumors notably improves the immune microenvironment, marked by increased PD-L1 expression and enhanced CD8⁺ T-cell infiltration, as well as elevated levels of CXCL9, CXCL10, and CXCL11. These changes promote antitumor T-cell immune responses and amplify the effects of immunotherapy. Mechanistic investiga

SUBMITTER: Wang S 

PROVIDER: S-EPMC12932977 | biostudies-literature | 2026 Mar

REPOSITORIES: biostudies-literature