Exploration of the role of <i>HNRNPA2B1</i> in keloid fibroblasts

ZHANG Luyang; WEI Xinggang; LI Siye; LIU Anzhu; LENG Xiangfeng

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

Volume 23 Issue 7

Jul. 2025

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Article Navigation > Chinese Journal of General Practice > 2025 > 23(7): 1130-1134

ZHANG Luyang, WEI Xinggang, LI Siye, LIU Anzhu, LENG Xiangfeng. Exploration of the role of HNRNPA2B1 in keloid fibroblasts[J]. Chinese Journal of General Practice, 2025, 23(7): 1130-1134. doi: 10.16766/j.cnki.issn.1674-4152.004081

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ZHANG Luyang, WEI Xinggang, LI Siye, LIU Anzhu, LENG Xiangfeng. Exploration of the role of HNRNPA2B1 in keloid fibroblasts[J]. Chinese Journal of General Practice, 2025, 23(7): 1130-1134. doi: 10.16766/j.cnki.issn.1674-4152.004081

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Exploration of the role of HNRNPA2B1 in keloid fibroblasts

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

ZHANG Luyang^{1, 2}
, WEI Xinggang³
, LI Siye²
, LIU Anzhu²
, LENG Xiangfeng^{1
,
,}

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

Funds:

ZR2021MH027

Received Date: 2024-12-25
Available Online: 2025-10-25

Abstract

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

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References(26)

References

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Exploration of the role of HNRNPA2B1 in keloid fibroblasts

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