<i>HNRNPA2B1</i>在瘢痕疙瘩成纤维细胞中的作用探究

张路阳; 魏兴罡; 李嗣晔; 刘桉助; 冷向锋

doi:10.16766/j.cnki.issn.1674-4152.004081

HNRNPA2B1在瘢痕疙瘩成纤维细胞中的作用探究

doi: 10.16766/j.cnki.issn.1674-4152.004081

张路阳^{1, 2},
魏兴罡³,
李嗣晔²,
刘桉助²,
冷向锋^1, ,

1.
青岛大学附属医院整形外科, 山东青岛 266071
2.
海军第九七一医院手外科, 山东青岛 266071
3.
阳泉煤业(集团)有限责任公司总医院手外科, 山西阳泉 045099

基金项目:

山东省自然科学基金面上项目 ZR2021MH027

详细信息

通讯作者:
冷向锋，E-mail：lxfzqcn@qdu.edu.cn

中图分类号: R619.6
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- 被引次数: 0
出版历程
- 收稿日期: 2024-12-25
- 网络出版日期: 2025-10-25

Exploration of the role of HNRNPA2B1 in keloid fibroblasts

1.
Plastic Surgery Department, Affiliated Hospital of Qingdao University, Qingdao, Shandong 266071, China

摘要

摘要: 目的瘢痕疙瘩是异常伤口愈合引发的纤维增生性疾病，m6A甲基化修饰是最常见的RNA修饰, 可调控RNA稳定。HNRNPA2B1作为m6A读取器已被证实参与多种肿瘤发生，但在瘢痕疙瘩中的作用及分子机制尚未明确。为此，本研究旨在探究HNRNPA2B1在瘢痕疙瘩中的具体作用及调控机制。方法利用来自基因表达综合(GEO)数据库的公开基因表达数据集，其中包含15个对照样本和14个瘢痕疙瘩患者样本，筛选出瘢痕成纤维细胞中的差异表达基因(DEGs)。数据预处理和批次校正后，通过全面分析，阐明DEGs的功能含义。通过基因敲除实验，探究HNRNPA2B1对瘢痕成纤维细胞行为的直接影响。结果通过对GSE7890和GSE145725数据集进行分析及注释，筛选出23个m6A相关基因，通过富集分析，发现HNRNPA2B1基因影响瘢痕成纤维细胞增殖及代谢。通过体外实验对HNRNPA2B1敲除，结果显示，相比对照组，HNRNPA2B1敲除能够显著抑制细胞的迁移。结论本研究通过生物信息学分析与体外实验证实，HNRNPA2B1作为m6A修饰读取器，在瘢痕疙瘩成纤维细胞中高表达并通过调控Wnt、P53、HIF-1等信号通路，能够调控细胞增殖、代谢及迁移过程。基因敲除实验显示，抑制HNRNPA2B1可显著降低细胞迁移能力，揭示了其在瘢痕疙瘩纤维化中的关键作用，为该疾病的分子机制解析及靶向治疗提供了新的研究方向。
- 瘢痕 /
- HNRNPA2B1 /
- 甲基化修饰
Abstract: Objective Keloid is a fibroproliferative disease triggered by abnormal wound healing, and N6-methyladenosine (m6A), as the most common RNA modification, can regulate RNA stability. Heterogeneous nuclear ribonucleoprotein A2B1 (HNRNPA2B1), as an m6A reader, has been confirmed to be involved in the tumorigenesis of multiple cancers, but its role and molecular mechanism in keloid remain unclear. Therefore, this study focuses on HNRNPA2B1 to explore its specific function and regulatory mechanism in keloid. Methods Using a publicly available gene expression dataset from the Gene Expression Omnibus (GEO) database, which includes 15 control samples and 14 keloid tissue patient samples, differentially expressed genes (DEGs) in keloid fibroblasts were screened. After data preprocessing and batch calibration, a comprehensive analysis was conducted to clarify the functional meaning of DEGs. In addition, this study investigated the direct effect of HNRNPA2B1 on the behavior of scar fibroblasts through gene knockout experiments. Results This study analyzed the GSE7890 and GSE145725 datasets identified the related functions of differentially expressed genes, screened out 23 m6A-related genes, and enrichment analysis revealed that the HNRNPA2B1 gene affects the proliferation and metabolism of scar fibroblasts. Through in vitro experiments, HNRNPA2B1 knockout was found to significantly inhibit cell migration compared to the control group. Conclusion This study confirmed through bioinformatics analysis and in vitro experiments that HNRNPA2B1, as an m6A modified reader, is highly expressed in keloid tissue fibroblasts and can regulate cell proliferation, metabolism, and migration processes by regulating signaling pathways such as Wnt, P53, and HIF-1. Gene knockout experiments have shown that inhibiting HNRNPA2B1 can significantly reduce cell migration ability, revealing its key role in scar tissue fibrosis and providing new research directions for molecular mechanism analysis and targeted therapy of this disease.
- Keloid /
- HNRNPA2B1 /
- Methylation modification

HTML全文

图 1 瘢痕与正常组织成纤维细胞差异分析

Figure 1. Differential analysis of fibroblasts between scar and normal tissues

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图 2 瘢痕与正常组织成纤维细胞m6A修饰相关基因差异比较

注：^aP＜0.05，^bP＜0.01。

Figure 2. Comparison of m6A-modification - related gene expression between scar and normal tissue fibroblasts

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图 3 HNRNPA2B1基因功能富集分析

Figure 3. Functional enrichment analysis of HNRNPA12B1 gene

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图 4 HNRNPA2B1敲除抑制细胞迁移能力

注：A为免疫印迹法验证敲除HNRNPA2B1效果及灰度定量；B为划痕试验检测Si-HNRNPA2B1的细胞迁移；^aP＜0.01。

Figure 4. Inhibitory effect of si-HNRNPA2B1 on scar fibroblast migration

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