Unveiling the role of m6A modification in esophageal cancer: a new frontier in tumor innate interferon immunity.

Esophageal cancer (ESCA) is one of the most common and aggressive malignancies worldwide and has a poor prognosis in its late stages, posing a significant threat to human health. N6-methyladenosine (m6A) is the most prevalent RNA chemical modification in eukaryotes, which has gained substantial attention for its critical role in regulating RNA stability, splicing, translation, and localization. Although m6A modification has been found implicated in the initiation and progression of various cancers, its specific mechanisms in ESCA remain underexplored. Concurrently, it’s well-recognized that innate immunity is the body’s first line of defense against pathogens, playing a vital role in tumor immune surveillance. Additionally, m6A modification has been shown to regulate multiple key innate immune signaling pathways, including the cGAS-STING, Toll-like receptor (TLR), and RIG-I-like receptor (RLR) pathways, which are integral to immune responses and closely linked to several diseases. However, the exact role of m6A in modulating these innate immune pathways in ESCA remains largely unclear. Therefore, this review aimed to explore the interplay between m6A modification and innate immune signaling in ESCA. The findings of this article may provide novel insights into the role of m6A in immune evasion and lay a solid foundation for developing novel immunotherapeutic strategies.