Overview
- Researchers report that under tumor stress MYC binds nascent RNA, forms multimers, and recruits the nuclear exosome to clear RNA–DNA hybrids known as R-loops.
- Elimination of these hybrids suppresses innate immune alarm pathways, including signaling through TLR3 and the kinase TBK1.
- In mouse models of pancreatic cancer, disabling a critical MYC RNA‑binding region caused tumors to shrink by 94% over 28 days, while tumors with normal MYC grew 24-fold, and the effect required an intact immune system.
- The RNA-binding function that drives immune evasion is mechanistically separate from MYC’s DNA-binding growth role, indicating a more precise therapeutic target than global MYC inhibition.
- Authors outline next steps to track nuclear export of R‑loop–derived signals and assess tumor‑microenvironment effects, noting that translation to human therapies remains at an early stage.