RNA editing as an epitranscriptomic immune switch in tumor immunity and cancer immunotherapy

RNA editing is a dynamically regulated posttranscriptional mechanism that expands transcriptomic diversity and modulates cellular phenotypes. Accumulating evidence indicates that RNA editing, particularly adenosine-to-inosine (A-to-I) and cytidine-to-uridine (C-to-U) editing, plays a critical role in shaping tumor–immune interactions. Emerging studies have demonstrated that dysregulated RNA editing contributes to tumor progression by impairing immune recognition, suppressing innate immune sensing, and remodeling the tumor microenvironment (TME). Mechanistically, RNA editing influences tumor immunity through multiple mechanisms, including protein recoding, the modulation of innate immune signaling pathways such as MDA5/MAVS, and interactions with other epitranscriptomic modifications, including N6-methyladenosine (m 6 A). Notably, recent advances in programmable RNA base editing technologies, such as engineered ADAR systems and Cas13-deaminase fusion-based editing platforms, and other RNA-targeting technologies have provided new tools for precise and transient regulation at the RNA level and have shown potential value in cancer immunotherapy. Moreover, the development of RNA delivery and expression platforms has further expanded the in vivo application possibilities of these strategies. However, these technologies differ significantly in terms of their mechanism and evidence maturity: programmable RNA editing directly alters the RNA nucleotide sequence, while Cas13-mediated RNA degradation, RNA processing, and RNA vaccines are not RNA base editing in the strict sense. Despite these advances, editing specificity, cell- and tissue-specific delivery, and biosafety remain major challenges for clinical translation. Overall, RNA editing is emerging as an important mechanism that can connect tumor immune regulation and precision RNA therapy, but further validation is needed before clinical application.