Oncogenic tRF-24-O7M8LO9LIM drives lung adenocarcinoma progression by disrupting the CD82/p53 tumor suppressor pathway.

Transfer RNA-derived small RNAs (tsRNAs), a recently identified class of non-coding RNAs, have been shown to play regulatory roles in various malignancies. However, their functions in lung adenocarcinoma (LUAD) remain largely unexplored. This study aims to elucidate the molecular mechanisms and biological functions of tRF-24-O7M8LO9LIM in LUAD. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to measure the expression levels of tRF-24-O7M8LO9LIM in LUAD patient tissues and lung cancer cell lines. Chi-square tests were performed to analyze the correlations between its expression and clinicopathological characteristics. Kaplan-Meier survival analysis was conducted to assess its prognostic significance. Plasmids for the knockdown and overexpression of tRF-24-O7M8LO9LIM were constructed, and their effects were validated through in vitro cell-based assays-including CCK-8, EdU, colony formation, and Transwell assays-as well as in vivo tumorigenicity experiments in nude mice. A dual-luciferase assay was employed to validate the relationship between tRF-24-O7M8LO9LIM and its downstream target genes. KEGG pathway analysis and western blotting were further used to validate the associated signaling pathways. The results showed that tRF-24-O7M8LO9LIM is highly expressed in LUAD patient tissues and lung cancer cells, correlates with TNM stage and tumor size, and has significant prognostic value. Knockdown of tRF-24-O7M8LO9LIM inhibited cellular proliferation, migration, and invasion in vitro, while simultaneously suppressing tumor growth in vivo. The dual-luciferase assay confirmed the direct binding between tRF-24-O7M8LO9LIM and its downstream target, CD82. KEGG pathway analysis and western blotting experiments demonstrated that tRF-24-O7M8LO9LIM regulates the p53 signaling pathway via CD82. In conclusion, tRF-24-O7M8LO9LIM promotes the progression of LUAD by targeting CD82 to regulate the p53 signaling pathway.