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

IF 3 3区生物学 Q3 BIOCHEMICAL RESEARCH METHODS

Molecular and Cellular Probes Pub Date : 2026-02-01 Epub Date: 2025-12-01 DOI:10.1016/j.mcp.2025.102057

Xin Chen, Weiqing Chen

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引用次数: 0

Abstract

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.

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揭示DDX10在弥漫性大b细胞淋巴瘤中的调节作用：与FBL结合促进细胞增殖和侵袭

背景：弥漫性大B细胞淋巴瘤（DLBCL）是一种分子病因不明的异质性恶性肿瘤。本研究旨在探讨一种新型致癌基因DEAD-box解旋酶10 （DDX10）在DLBCL中的作用。方法采用GEPIA2生物信息学工具分析DDX10在DLBCL中的表达。采用实时定量逆转录聚合酶链反应检测DLBCL患者肿瘤组织和细胞系中DDX10和纤原蛋白（FBL）的表达。RNA免疫沉淀法证实FBL-DDX10相互作用。研究了DDX10/FBL过表达和敲低对DLBCL细胞活力、侵袭性和Wnt/β-catenin通路蛋白的影响。结果ddx10和FBL在DLBCL患者中表达水平升高，特别是在III期或IV期DLBCL患者中。DDX10可与DLBCL细胞中的FBL结合。DDX10或FBL的沉默抑制了DLBCL细胞的活力、增殖和侵袭，下调了β-catenin、cyclin D1和c-Myc蛋白的表达。DDX10或FBL沉默对DLBCL细胞的调控作用被FBL或DDX10的过表达所抵消。结论ddx10通过正调控FBL参与DLBCL细胞的增殖和侵袭，提示DDX10-FBL轴可能是潜在的治疗靶点。这项工作为DLBCL的发病机制提供了新的见解，并强调了靶向DDX10-FBL的生物医学相关性。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Molecular and Cellular Probes 生物-生化研究方法

CiteScore

6.80

自引率

0.00%

发文量

审稿时长

16 days

期刊介绍： MCP - Advancing biology throughâ€“omics and bioinformatic technologies wants to capture outcomes from the current revolution in molecular technologies and sciences. The journal has broadened its scope and embraces any high quality research papers, reviews and opinions in areas including, but not limited to, molecular biology, cell biology, biochemistry, immunology, physiology, epidemiology, ecology, virology, microbiology, parasitology, genetics, evolutionary biology, genomics (including metagenomics), bioinformatics, proteomics, metabolomics, glycomics, and lipidomics. Submissions with a technology-driven focus on understanding normal biological or disease processes as well as conceptual advances and paradigm shifts are particularly encouraged. The Editors welcome fundamental or applied research areas; pre-submission enquiries about advanced draft manuscripts are welcomed. Top quality research and manuscripts will be fast-tracked.