ORIGINAL RESEARCH article
Front. Oncol.
Sec. Cancer Imaging and Image-directed Interventions
This article is part of the Research TopicAdvancing Cancer Imaging Technologies: Bridging the Gap from Research to Clinical Practice Volume IIView all 13 articles
MiR-10a-5p Suppresses Hepatocellular Carcinoma Progression and Microvascular Invasion by Targeting TFR1-STAT3-CD24 Signaling Axis
Provisionally accepted
- 1Guilin Medical University, Guilin, China
- 2Liuzhou People's Hospital, Liuzhou, China
- 3Canon Medical Systems Kabushiki Kaisha, Otawara, Japan
- 4Guangxi Medical University Cancer Hospital, Nanning, China
Select one of your emails
You have multiple emails registered with Frontiers:
Notify me on publication
Please enter your email address:
If you already have an account, please login
You don't have a Frontiers account ? You can register here
Background: Preoperative CT features have demonstrated potential in predicting microvascular invasion (MVI) in hepatocellular carcinoma. These CT signs serve as indicators of tumor biological behavior. However, the molecular mechanisms underlying the ability of CT to preoperatively predict MVI remain largely unexplored. This study aims to elucidate the role of miR-10a-5p in HCC progression and investigate its correlation with specific imaging features. Methods: According to preoperative CT features, patients were divided into CT-MVI (+) group and CT-MVI (-) group. MiR-10a-5p expression was analyzed in HCC tissues with CT-MVI compared to those without CT-MVI. The functional effects of miR-10a-5p were assessed through in vitro cell viability and apoptosis assays, and in vivo xenograft models. Cell viability was assessed through the CCK8 assay, while flow cytometry was utilized to determine cell apoptosis. The regulatory relationships between miR-10a-5p, CD24, transferrin receptor 1 (TFR1), and STAT3 signaling were explored using western blot, luciferase reporter assays, and rescue experiments. Results: MiR-10a-5p expression was significantly downregulated in HCC tissues with CT-MVI compared to those without CT-MVI. Overexpression of miR-10a-5p reduced cell viability, promoted apoptosis, and inhibited tumor growth in vivo. MiR-10a-5p directly targeted TFR1, leading to decreased CD24 expression and reduced STAT3 phosphorylation. TFR1 overexpression partially rescued the effects of miR-10a-5p on cell apoptosis and CD24 expression. Conclusions: Our findings reveal miR-10a-5p as a key regulator of HCC progression and MVI, operating through a novel pathway involving TFR1, STAT3, and CD24. This study provides new insights into the molecular mechanisms of CT features and highlights potential therapeutic targets for HCC treatment.
Keywords: Hepatocellular Carcinoma, CT, MiR-10a-5p, CD24, Transferrin receptor 1, stat3
Received: 28 Aug 2025; Accepted: 01 Dec 2025.
Copyright: © 2025 Zhang, Lai, Wang, Nong, Chen, Xu, Bai and Zhang. 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:
Yupeng Zhang
Tao Bai
Wei Zhang
Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.