ANLN knockdown inhibits nasopharyngeal carcinoma proliferation and is associated with impaired ribosome biogenesis.

Anillin (ANLN), an actin-binding protein, has been implicated in tumorigenesis across various cancers; however, its role in nasopharyngeal carcinoma (NPC) remains largely undefined. In this study, we analyzed ANLN expression using TCGA, CPTAC, and GEO datasets, and confirmed its overexpression in NPC tissues and cell lines through qRT-PCR, western blotting, and immunohistochemistry. High ANLN expression correlated with advanced clinical stage and poor overall survival. Functional assays, including CCK-8 and colony formation, demonstrated that ANLN knockdown suppressed NPC cell proliferation in vitro, while xenograft models confirmed reduced tumor growth in vivo. RNA sequencing and gene set enrichment analysis revealed that ANLN knockdown was associated with downregulation of ribosome biogenesis pathways. Puromycin incorporation assays and transmission electron microscopy further supported impaired protein synthesis and nucleolar disruption following ANLN depletion. These findings suggest that ANLN promotes NPC progression by maintaining ribosome biogenesis and protein synthesis and may serve as a novel prognostic biomarker and therapeutic target.