BEND3 promotes hepatocellular carcinoma progression and metastasis by activating the PI3K/AKT/mTOR pathway and inducing epithelial-mesenchymal transition.
Liu-Lin Yang, Xing Chen, Kai-Ting Huang, Shao-Tong Tang, Gui-Yan Ye, Ji-Long Wang
{"title":"BEND3 promotes hepatocellular carcinoma progression and metastasis by activating the PI3K/AKT/mTOR pathway and inducing epithelial-mesenchymal transition.","authors":"Liu-Lin Yang, Xing Chen, Kai-Ting Huang, Shao-Tong Tang, Gui-Yan Ye, Ji-Long Wang","doi":"10.1016/j.clinre.2025.102582","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>This study aimed to investigate the expression of BEND3 in hepatocellular carcinoma (HCC), its correlation with clinical characteristics, and its functional and mechanistic impacts on HCC progression.</p><p><strong>Methods: </strong>Bioinformatics analyses identified BEND3 as highly expressed in HCC and associated with poor clinical prognosis, which was further validated using qRT-PCR, western blotting and immunohistochemistry. Stable BEND3-overexpressing and silenced cell lines were constructed to evaluate its functional effects. CCK-8 and colony formation assays assessed its influence on cell proliferation, while wound healing and Transwell assays evaluated its role in migration and invasion. WB and immunofluorescence were employed to analyze the effects of BEND3 on epithelial-mesenchymal transition (EMT) and the PI3K/AKT/mTOR signaling pathway.</p><p><strong>Results: </strong>Public database analysis, alongside qRT-PCR, western blotting, and immunohistochemical, confirmed that BEND3 expression is significantly elevated in HCC tissues compared to normal liver tissues and is closely associated with poor prognosis. Functional assays demonstrated that BEND3 promotes HCC cell proliferation, migration, and invasion. Mechanistic studies revealed that BEND3 drives HCC progression by inducing EMT and activating the PI3K/AKT/mTOR signaling pathway.</p><p><strong>Conclusion: </strong>BEND3 is highly expressed in HCC and strongly correlates with poor clinical outcomes. Functional and mechanistic analyses indicate that BEND3 enhances HCC progression by promoting proliferation, migration and invasion via EMT induction and PI3K/AKT/mTOR pathway activation.</p>","PeriodicalId":10424,"journal":{"name":"Clinics and research in hepatology and gastroenterology","volume":" ","pages":"102582"},"PeriodicalIF":2.6000,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Clinics and research in hepatology and gastroenterology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1016/j.clinre.2025.102582","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"GASTROENTEROLOGY & HEPATOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Objective: This study aimed to investigate the expression of BEND3 in hepatocellular carcinoma (HCC), its correlation with clinical characteristics, and its functional and mechanistic impacts on HCC progression.
Methods: Bioinformatics analyses identified BEND3 as highly expressed in HCC and associated with poor clinical prognosis, which was further validated using qRT-PCR, western blotting and immunohistochemistry. Stable BEND3-overexpressing and silenced cell lines were constructed to evaluate its functional effects. CCK-8 and colony formation assays assessed its influence on cell proliferation, while wound healing and Transwell assays evaluated its role in migration and invasion. WB and immunofluorescence were employed to analyze the effects of BEND3 on epithelial-mesenchymal transition (EMT) and the PI3K/AKT/mTOR signaling pathway.
Results: Public database analysis, alongside qRT-PCR, western blotting, and immunohistochemical, confirmed that BEND3 expression is significantly elevated in HCC tissues compared to normal liver tissues and is closely associated with poor prognosis. Functional assays demonstrated that BEND3 promotes HCC cell proliferation, migration, and invasion. Mechanistic studies revealed that BEND3 drives HCC progression by inducing EMT and activating the PI3K/AKT/mTOR signaling pathway.
Conclusion: BEND3 is highly expressed in HCC and strongly correlates with poor clinical outcomes. Functional and mechanistic analyses indicate that BEND3 enhances HCC progression by promoting proliferation, migration and invasion via EMT induction and PI3K/AKT/mTOR pathway activation.
期刊介绍:
Clinics and Research in Hepatology and Gastroenterology publishes high-quality original research papers in the field of hepatology and gastroenterology. The editors put the accent on rapid communication of new research and clinical developments and so called "hot topic" issues. Following a clear Editorial line, besides original articles and case reports, each issue features editorials, commentaries and reviews. The journal encourages research and discussion between all those involved in the specialty on an international level. All articles are peer reviewed by international experts, the articles in press are online and indexed in the international databases (Current Contents, Pubmed, Scopus, Science Direct).
Clinics and Research in Hepatology and Gastroenterology is a subscription journal (with optional open access), which allows you to publish your research without any cost to you (unless you proactively chose the open access option). Your article will be available to all researchers around the globe whose institution has a subscription to the journal.