BUD23 is associated with malignancy and correlates with immune infiltration in NSCLC

Lung cancer remains the primary cause of cancer‑related mortality worldwide. BUD23, also known as Williams‑Beuren syndrome critical region 22, is an rRNA methyltransferase involved in ribosome maturation and RNA methylation. It has been reported to promote tumor progression in several malignancies. Although BUD23 has been implicated in drug resistance in lung cancer cells, its role in non‑small cell lung cancer (NSCLC) remains incompletely understood. In the present study, transcriptomic and proteomic datasets were analyzed to evaluate the expression of BUD23 in NSCLC and normal tissues, and Kaplan‑Meier survival analysis was performed to assess its prognostic significance. Immune infiltration algorithms were used to examine the correlation between BUD23 expression and tumor immune cell infiltration in NSCLC. Gene set enrichment analysis (GSEA), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis and single‑cell enrichment analysis were conducted to explore the biological pathways associated with BUD23 expression. In vitro, the effect of BUD23 knockdown on the viability, motility and apoptosis of NSCLC cell lines was evaluated by Cell Counting Kit‑8, wound healing and Annexin V/PI flow cytometry assays, respectively, and the mRNA expression levels of potential downstream genes were quantified by reverse transcription‑quantitative PCR. BUD23 was found to be significantly upregulated in NSCLC and associated with poor patient survival. Immunogenomic analyses indicated that high BUD23 levels are correlated with reduced immune cell infiltration. GSEA, KEGG and single‑cell pathway enrichment analyses consistently implicated BUD23 in ‘DNA repair’ and ‘cell cycle’ pathways. In vitro, BUD23 knockdown suppressed the proliferation and migration of NSCLC cells, and reduced RNA polymerase II subunit J expression. Collectively, these findings suggest that BUD23 may contribute to the development and progression of NSCLC, and provide a strong basis for future mechanistic and clinical investigations.