Fig. 7: A mechanism schematic diagram of tRF-Ser-mediated tumor suppression in GC.

tRF-Ser binds to the transcription factor CNBP and promotes its accumulation in the cytoplasm, thereby repressing CNBP-mediated transcriptional activation of HSPA8. Then, the tRF-Ser/CNBP/HSPA8 axis suppresses β-catenin-mediated EMT and induces GPX4 ubiquitination-dependent ferroptosis to inhibit GC progression.