TRF-16 Inhibits Lung Cancer Progression by Hindering the N6-Methyladenosine Modification of CPT1A mRNA

Transfer RNA-derived fragments (tRFs) are a new class of small non-coding RNAs. Recent studies suggest that tRFs participate in some pathological processes. However, the biological activities and processes of tRFs in lung cancer cells remain mainly unclear. In the present investigation, we employed tRNA-derived small RNA (tsRNA) sequencing to predict differentially expressed tsRNAs in lung cancer cells, and nine tsRNAs with significant expression alterations were validated using qPCR. Wound healing, colony formation, transwell invasion and CCK-8 assays were performed to detect the effects of tRF-16 on cell function. Western blotting evaluated the relationship between tRF-16 and the IGF2BP1 axis. Our findings demonstrated that tRF-16 expression was substantially downregulated in lung cancer cells. TRF-16 could inhibit lung cancer cells' ability to increase, migrate, invade and obtain radiation resistance. Furthermore, tRF-16 decreases the stability of CPT1A by impairing the binding of IGF2BP1 to CPT1A. As a result, the fatty acid metabolism in lung cancer cells was inhibited. Finally, tRF-16 also inhibits lung cancer cell proliferation in vivo. This study shows that tRF-16 plays a crucial regulatory role in the proliferation of lung cancer cells and may represent a novel avenue for their regulation.