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

Carcinogenesis, Teratogenesis & Mutagenesis ›› 2025, Vol. 37 ›› Issue (6): 452-457.doi: 10.3969/j.issn.1004-616x.2025.06.005

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

Abstract

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

CLC Number:

R285.5

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

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