MicroRNA-23C Impacts Hepatocellular Carcinoma Metastasis by Targeting OTUB1
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BACKGROUND: MicroRNA-23C (miR-23C) and Ovarian Tumor domain-containing Ubiquitin Aldehyde-Binding protein 1 (OTUB1) have been crucially implicated in numerous malignancies, such as Hepatocellular Carcinoma (HCC), a common malignant tumor. Herein, the function of the miR-23C-OTUB1-PI3K/AKT signaling pathway in HCC cell aggressiveness and Epithelial-Mesenchymal Transition (EMT) was explored, potentially revealing novel therapeutic approaches or targets for HCC. METHODS: miR-23C expression was predicted and confirmed using bioinformatics analysis and Real-Time Quantitative Polymerase Chain Reaction (RT-qPCR), respectively. The findings suggest miR-23C suppression was evaluated via the Cell Counting Kit 8 (CCK8), Transwell invasion, and wound healing assays. Western Blotting (WB) was employed to analyze EMT-related protein expression and the phosphorylation level of AKT (AK strain transforming). Target genes and binding sites were predicted using bioinformatics analysis, and their validation was confirmed by a dual-luciferase assay. The in vivo regulatory impact of miR-23C on target genes was confirmed using a model of nude mouse xenograft. RESULTS: Both HCC tissues and cells exhibited miR-23C downregulation. While OTUB1 overexpression promoted HCC cell invasion, migration, and EMT, its knockdown, along with miR-23C upregulation, exerted a contrary effect. We further identified OTUB1 as a target gene of miR-23C, and in vivo experiments confirmed that miR-23C negatively regulated OTUB1 expression. Additionally, OTUB1 overexpression increased AKT phosphorylation, a phenomenon that was inhibited by OTUB1 silencing or transfection with the miR-23C mimic. Moreover, co-overexpression of OTUB1 and the miR-23C mimic counteracted the OTUB1 effects. DISCUSSION: Our findings show miR-23C may suppress Hepatocellular Carcinoma (HCC) metastasis in experimental models by directly targeting OTUB1, potentially contributing to the inactivation of the PI3K/AKT pathway. These preliminary findings suggest that the miR-23C/OTUB1/AKT axis may warrant further investigation as a potential therapeutic target. CONCLUSION: Overall, in our preclinical models, miR-23C appeared to inhibit HCC cell aggressiveness and EMT by targeting OTUB1 and potentially regulating the PI3K/AKT pathway.
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Le contrôle bibliographique ouvert
DOI retrouvé dans Crossref DOI retrouvé ; titre concordant.
- Titre Crossref
- MicroRNA-23C Impacts Hepatocellular Carcinoma Metastasis by Targeting OTUB1
- Date Crossref
- 09/09/2026
- Éditeur
- Bentham Science Publishers Ltd.
- Type
- journal-article
Ce recoupement confirme des métadonnées liées au DOI. Il ne confirme ni la méthode ni les conclusions de l’étude, et il ne compte pas comme une seconde source scientifique indépendante.
Où se fait cette recherche
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Yancheng Third People's Hospital pays non établi dans la noticeÉtablissement de santé
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Yancheng Second People's Hospital Department of Radiology pays non établi dans la noticeÉtablissement de santé
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Xuzhou Medical College pays non établi dans la noticeUniversité ou école supérieure
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Nantong University Department of Central Laboratory pays non établi dans la noticeUniversité ou école supérieure
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Yancheng First People's Hospital pays non établi dans la noticeÉtablissement de santé
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Jiamusi University pays non établi dans la noticeUniversité ou école supérieure
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Heilongjiang Academy of Agricultural Machinery Engineering pays non établi dans la noticeStructure de recherche
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The Yancheng Clinical College of Xuzhou Medical University Department of Burn and Plastic Surgery pays non établi dans la noticeUniversité ou école supérieure
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College of pharmacy pays non établi dans la noticeUniversité ou école supérieure
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Heilongjiang Pharmaceutical Research Institute pays non établi dans la noticeStructure de recherche
Yancheng Third People's Hospital, Department of Radiology — Yancheng Second People's Hospital et Xuzhou Medical College, avec 7 autres affiliations.
Une affiliation ne permet pas de déduire la nationalité d’un auteur.