Reveal the regulatory role of DDX10 in diffuse large B-cell lymphoma: binding with FBL to promote cell proliferation and invasion.

[BACKGROUND] Diffuse large B cell lymphoma (DLBCL) is a heterogeneous malignancy with an unidentified molecular etiology. This study aims to investigate the role of DEAD-box helicase 10 (DDX10), a novel carcinogenic gene, in DLBCL.

[METHODS] The expression of DDX10 in DLBCL was analyzed by the GEPIA2 bioinformatics tool. DDX10 and fibrillarin (FBL) expressions in DLBCL patients' cancer tissues and cell lines were measured via quantitative real-time reverse transcription polymerase chain reaction. RNA immunoprecipitation assay was used to confirm FBL-DDX10 interaction. The effects of DDX10/FBL overexpression and knockdown on cell viability, invasion, and Wnt/β-catenin pathway proteins were evaluated in DLBCL cell lines.

[RESULTS] DDX10 and FBL exhibited elevated expression levels in patients with DLBCL, particularly in those with stage III or IV DLBCL. DDX10 can bind to FBL in DLBCL cells. Silencing of DDX10 or FBL suppressed viability, proliferation and invasion, and downregulated the expressions of β-catenin, cyclin D1, and c-Myc proteins in DLBCL cells. The regulatory impact of DDX10 or FBL silencing on DLBCL cells was counteracted by the overexpression of FBL or DDX10.

[CONCLUSION] DDX10 contributes to the proliferation and invasion of DLBCL cells via positively regulating FBL, highlighting the DDX10-FBL axis as a potential therapeutic target. This work provides new insights into DLBCL pathogenesis and underscores the biomedical relevance of targeting DDX10-FBL.