Effects of RPL37 on the proliferation, migration, and invasion of non–small cell lung cancer cells.

e20513 Background: Non-small cell lung cancer (NSCLC) remains a leading cause of cancer-related mortality worldwide. Despite advances in targeted therapy and immunotherapy, overall prognosis remains poor, underscoring the need to better understand the molecular drivers of tumor progression. Ribosomal proteins, including ribosomal protein L37 (RPL37), have been implicated in extra-ribosomal oncogenic functions in several cancers, but their role in NSCLC is unclear. This study aimed to investigate the function and mechanism of RPL37 in NSCLC pathogenesis. Methods: Bioinformatics analysis of TCGA data assessed RPL37 expression in NSCLC. RPL37 was modulated in A549, H1299, and PC9 cell lines via siRNA/plasmid transfection and lentiviral knockdown. Functional assays included colony formation, wound healing, and Transwell migration/invasion. EMT markers (E-cadherin, ZO-1, N-cadherin, Vimentin, Snail) and Wnt/β-catenin pathway components (cyclin D1, β-catenin, MMP9, c-myc) were analyzed by Western blot. Subcutaneous xenograft models in nude mice evaluated tumor growth in vivo. Transcriptome sequencing identified potential downstream pathways. Results: We found that RPL37 is upregulated in NSCLC tissues compared to adjacent normal tissues. Using loss-of-function and gain-of-function approaches in A549, PC9, and H1299 cell lines, we demonstrated that RPL37 promotes NSCLC cell proliferation, migration, and invasion in vitro, and facilitates epithelial-mesenchymal transition (EMT). In vivo, RPL37 knockdown significantly inhibited tumor growth in a subcutaneous xenograft model. Mechanistically, transcriptome sequencing and western blotting revealed that RPL37 regulates key components of the Wnt/β-catenin pathway, including cyclin D1, β-catenin, MMP9, and c-myc. Conclusions: Collectively, our findings indicate that RPL37 functions as an oncoprotein in NSCLC by enhancing malignant phenotypes through activation of the Wnt/β-catenin signaling pathway. RPL37 may thus represent a potential therapeutic target for NSCLC intervention.