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ORIGINAL RESEARCH article

Front. Oncol.

Sec. Molecular and Cellular Oncology

Volume 15 - 2025 | doi: 10.3389/fonc.2025.1576449

Identification of Key Molecular Targets for Stachyose in Hepatocellular Carcinoma: Focus on STAT3 and FN1

Provisionally accepted
Haihua  ChenHaihua Chen1Xianyou  WangXianyou Wang1Jiongcheng  YingJiongcheng Ying2Yuqin  HuangYuqin Huang2Yuxi  LiuYuxi Liu2Yifu  FengYifu Feng3Binbo  FangBinbo Fang2*
  • 1Zhejiang Taizhou Hospital, Taizhou, Zhejiang Province, China
  • 2Taizhou University, Taizhou, China
  • 3Taizhou Central Hospital, Taizhou, China

The final, formatted version of the article will be published soon.

Background and Objective: Hepatocellular carcinoma (HCC) ranks among the most prevalent malignancies on a global scale. Stachyose (STA), an oligosaccharide widely present in legumes, has demonstrated various biological activities, including improving gut microbiota, anti-oxidative stress, and anti-tumor proliferation. This study aimed to predict potential targets of STA in HCC treatment and to identify key hub genes. Methods: By integrating multiple public databases and bioinformatics tools, we screened 34 candidate targets and constructed STA's action network and PPI network in HCC. Functional enrichment analysis revealed 10 relevant KEGG pathways and key features related to cellular components, molecular functions, and biological processes. Finally, we conducted molecular docking, single gene analysis, and in vitro experimental validation on core targets.Results: Through screening of multiple databases, we identified 34 common targets associated with STA and HCC and subsequently constructed a protein-protein interaction (PPI) network. Through this analysis, we ultimately selected STAT3 and FN1 as core hub genes. Functional and pathway analyses indicated that these targets participate in multiple cancer-related pathways and have significant roles in cellular components, biological processes, and molecular functions. The results indicated a positive correlation between the expression of STAT3 and FN1 with angiogenesis, tumor inflammation, and epithelial-mesenchymal transition (EMT). Molecular docking experiments validated the stable binding capacity between STA and these core genes, and in vitro experiments further confirmed that STA could inhibit HCC cell proliferation and migration by downregulating STAT3 and FN1 expression.Conclusion: This study offers a comprehensive exploration of the molecular mechanisms through which STA may treat HCC, identifying STAT3 and FN1 as key targets and validating their clinical relevance and potential for application.

Keywords: Stachyose, Hepatocellular Carcinoma, stat3, FN1, JAK

Received: 14 Feb 2025; Accepted: 08 Jul 2025.

Copyright: © 2025 Chen, Wang, Ying, Huang, Liu, Feng and Fang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Binbo Fang, Taizhou University, Taizhou, China

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