基于转录组测序技术探究没食子酸体外抗Burkitt淋巴瘤的分子机制

doi:10.3969/j.issn.1004-616x.2025.06.005

癌变·畸变·突变 ›› 2025, Vol. 37 ›› Issue (6): 452-457.doi: 10.3969/j.issn.1004-616x.2025.06.005

• 论著 • 上一篇

基于转录组测序技术探究没食子酸体外抗Burkitt淋巴瘤的分子机制

罗志强¹, 史甲儒², 王晨³, 张硕⁴, 崔悦², 李婧铭³, 于国华²

1. 中国中医科学院中药资源中心, 道地药材品质保障与资源持续利用全国重点实验室, 北京 100700;
2. 北京中医药大学生命科学学院, 北京 102488;
3. 北京中医药大学中药学院, 北京 102488;
4. 北京中医药大学中医学院, 北京 102488

收稿日期:2025-04-09 修回日期:2025-08-25 发布日期:2025-12-06
通讯作者: 于国华，E-mail：ghyu@bucm.edu.cn
作者简介:罗志强，E-mail：luozhiqiang@nrc.ac.cn。
基金资助:
国家自然科学基金青年科学基金项目(82404936)；中央级公益性科研院所基本科研业务费(ZZXT202402，ZZXT202415，ZZ2024030，ZZ16-YQ-044)

Exploring the molecular mechanism of gallic acid against Burkitt lymphoma in vitro based on transcriptome sequencing technology

LUO Zhiqiang¹, SHI Jiaru², WANG Chen³, ZHANG Shuo⁴, CUI Yue², LI Jingming³, YU Guohua²

1. State Key Laboratory for Quality Ensurance and Sustainable Use of Dao-di Herbs, National Resource Center for Chinese Materia Medica, China Academy of Chinese Medical Sciences, Beijing 100700;
2. School of Life Sciences, Beijing University of Chinese Medicine, Beijing 102488;
3. School of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing 102488;
4. School of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing 102488, China

Received:2025-04-09 Revised:2025-08-25 Published:2025-12-06

摘要/Abstract

摘要： 目的：基于转录组测序技术，探究没食子酸(GA)在体外抗Burkitt淋巴瘤的作用及其潜在分子机制。方法：通过CCK-8及PrestoBlue实验评估0、10、50和100 μmol/L GA对人淋巴瘤Raji细胞的增殖抑制作用，利用转录组测序技术结合差异表达分析、功能注释和通路富集分析，解析其作用机制，并通过实时荧光定量PCR(RT-qPCR)验证关键基因表达。结果：与对照组相比，CCK-8和PrestoBlue实验结果表明，50和100 μmol/L GA对Raji细胞增殖活性具有显著抑制作用(P<0.05或P<0.01)。通过转录组学分析进一步揭示，GA主要通过调控Fc γ受体介导的吞噬作用通路发挥其抗肿瘤效应。RT-qPCR实验结果表明，与对照组相比，100 μmol/L GA可显著抑制该通路关键调控基因VAV3、IGHG2、IGHV3-33的表达水平(P<0.05或P<0.01)，与转录组测序结果一致。结论：GA不仅具有一定的直接细胞毒性，还可能通过调控肿瘤细胞表面受体，增强免疫细胞对肿瘤细胞的识别和吞噬能力。

关键词: 没食子酸, Burkitt淋巴瘤, 转录组, 分子机制

Abstract: OBJECTIVE：To use the transcriptome sequencing technology to investigate molecular mechanism of gallic acid (GA) against Burkitt lymphoma in vitro. METHODS：Inhibitory effect of GA on proliferation of human lymphoma Raji cells was assessed using the CCK-8 and PrestoBlue assays. Transcriptome sequencing technology was employed，combined with differential expression analysis，functional annotation，and pathway enrichment analysis，to decipher its mechanism of action. Key gene expression was validated by quantitative real-time PCR (RT-qPCR). RESULTS：Compared with the control group，both CCK-8 and PrestoBlue assays indicated that 50 and 100 μmol/L GA significantly inhibited the proliferation activity of Raji cells (P<0.05 or P<0.01). Transcriptomic analysis further revealed that GA exerted its anti-proliferation effects primarily by regulating the Fcγ receptor-mediated phagocytosis pathway. RT-qPCR results demonstrated that 100 μmol/L GA significantly suppressed the expression levels of key regulatory genes (VAV3，IGHG2，IGHV3-33) in this pathway (P<0.05 or P<0.01)，which was consistent with the transcriptome sequencing results. CONCLUSION：GA not only demonstrated direct cytotoxic effects but also enhanced the recognition and phagocytosis of tumor cells through modulation of tumor cell surface receptors.

Key words: gallic acid, Burkitt lymphoma, transcriptome, molecular mechanisms

中图分类号:

R285.5

罗志强, 史甲儒, 王晨, 张硕, 崔悦, 李婧铭, 于国华. 基于转录组测序技术探究没食子酸体外抗Burkitt淋巴瘤的分子机制[J]. 癌变·畸变·突变, 2025, 37(6): 452-457.

LUO Zhiqiang, SHI Jiaru, WANG Chen, ZHANG Shuo, CUI Yue, LI Jingming, YU Guohua. Exploring the molecular mechanism of gallic acid against Burkitt lymphoma in vitro based on transcriptome sequencing technology[J]. Carcinogenesis, Teratogenesis & Mutagenesis, 2025, 37(6): 452-457.

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基于转录组测序技术探究没食子酸体外抗Burkitt淋巴瘤的分子机制

Exploring the molecular mechanism of gallic acid against Burkitt lymphoma in vitro based on transcriptome sequencing technology

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