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World J Gastrointest Oncol. Aug 15, 2026; 18(8): 119834
Published online Aug 15, 2026. doi: 10.4251/wjgo.119834
MCM10 promotes hepatocellular carcinoma progression through cyclin D1 regulation
Yi-Ru Chen, Gang Wang, Long-Jun He, Huo-Wang Ye, Li-Feng Wang, Dan-Dan Zou, Mei-Qian Wang, Hui-Wen Xie, Sen-Lin Zhu, Xin-Ying Wang
Yi-Ru Chen, Huo-Wang Ye, Li-Feng Wang, Dan-Dan Zou, Hui-Wen Xie, Xin-Ying Wang, Department of Gastroenterology, Zhujiang Hospital of Southern Medical University, Guangzhou 510280, Guangdong Province, China
Gang Wang, Department of Transfusion Medicine, Zhujiang Hospital of Southern Medical University, Guangzhou 510280, Guangdong Province, China
Long-Jun He, Department of Endoscopy, Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangdong Esophageal Cancer Institute, Guangzhou 510060, Guangdong Province, China
Mei-Qian Wang, Department of Gastroenterology, Shandong Provincial Hospital, Jinan 510280, Shandong Province, China
Sen-Lin Zhu, Department of Gastroenterology and Hepatology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, Guangdong Province, China
Co-first authors: Yi-Ru Chen and Gang Wang.
Co-corresponding authors: Sen-Lin Zhu and Xin-Ying Wang.
Author contributions: Chen YR and Wang G conceived, designed, and performed the experiments, analyzed the data, and drafted the manuscript; He LJ collected samples, performed experiments and prepared the manuscript; Ye HW and Wang LF analyzed the data and made revisions; Zou DD, Wang MQ and Xie HW provided crucial technical support; Wang XY and Zhu SL contributed to study design and revised the article. All authors read and approved the final manuscript. Chen YR and Wang G contributed equally as co-first authors. Wang XY and Zhu SL are designated as co-corresponding authors of this manuscript. Both authors contributed equivalently and substantially to this study. Wang XY was responsible for study conception, experimental design, and supervision of in vitro and in vivo experiments. Zhu SL provided critical clinical resources, pathological materials, data interpretation, and critical revision of the intellectual content. They jointly coordinated the research progress, addressed the reviewers’ comments, and take equal responsibility for the integrity of the entire study. Therefore, both authors qualify and deserve co-corresponding authorship.
Supported by Science and Technology Program of Guangzhou, No. 2024A04J4877; Clinical Research Special Fund of Guangdong Medical Association, No. 2024HY-A5018; the President Foundation of Zhujiang Hospital, Southern Medical University, No. Yzjj2022qn13; and Shandong Provincial Natural Science Foundation, No. ZR2024QH338.
Institutional review board statement: This study was approved by the Ethics Committee of Zhujiang Hospital of Southern Medical University, No. 2023-KY-318-01.
Institutional animal care and use committee statement: All procedures involving animals were conducted in accordance with the National Institutes of Health (NIH) Guide for the Care and Use of Laboratory Animals and were approved by Zhujiang Hospital of Southern Medical University, China. This study was designed to minimize animal suffering and ensure their humane treatment in compliance with all applicable federal, state, and institutional regulations. Animals were housed in accordance with the guidelines of Zhujiang Hospital of Southern Medical University Animal Care Facility, and all efforts were made to reduce the number of animals used and to refine the experimental procedures.
Conflict-of-interest statement: No authors have any conflict of interest.
ARRIVE guidelines statement: The authors have read the ARRIVE guidelines, and the manuscript was prepared and revised according to the ARRIVE guidelines.
Data sharing statement: The datasets used and/or analyzed during the current study are available from the corresponding author on reasonable request.
Corresponding author: Xin-Ying Wang, Department of Gastroenterology, Zhujiang Hospital of Southern Medical University, No. 253 Gongye Road, Guangzhou 510280, Guangdong Province, China.
helenwxy@smu.edu.cn
Received: February 7, 2026
Revised: February 19, 2026
Accepted: May 6, 2026
Published online: August 15, 2026
Processing time: 178 Days and 14.8 Hours
BACKGROUND
Eukaryotic DNA replication constitutes a core mechanism underlying cellular proliferation, whereas unrestrained DNA replication is widely recognized as a key driver of tumorigenesis. MCM10 plays an essential role in the initiation of DNA replication.
AIM
To explore the biological function of MCM10 in the progression of hepatocellular carcinoma (HCC).
METHODS
Immunohistochemical staining and large-scale data mining were employed to assess the association between MCM10 expression and clinical pathological characteristics in HCC. Furthermore, in vitro and in vivo experiments were performed to investigate the biological roles and underlying molecular mechanisms of MCM10 in HCC.
RESULTS
Elevated MCM10 expression was significantly associated with adverse clinicopathological features in HCC. High MCM10 expression levels predicted poorer clinical outcomes among patients with HCC. Functionally, upregulation of MCM10 significantly accelerated cellular proliferation in vitro and tumor formation in vivo. Conversely, MCM10 knockdown markedly suppressed HCC cell proliferation and oncogenic activity. Mechanistic investigations revealed that MCM10 promoted cell cycle progression by activating the cyclin D1-CDK4/6 signaling axis. Notably, time-dependent receiver operating characteristic curve analysis demonstrated that the combined detection of MCM10 and cyclin D1 exhibited a consistently modest advantage over either marker alone in predicting patient survival throughout the observation period.
CONCLUSION
MCM10 facilitates HCC progression by activating the cyclin D1-CDK4/6 pathway, supporting a synergistic prognostic significance of the MCM10-cyclin D1 signature for HCC.
Core Tip: DNA replication constitutes a core mechanism underlying cell proliferation, whereas unrestrained DNA replication is a pivotal driving force in tumorigenesis. This study aimed to explore the biological function of the conserved replication regulator MCM10 in hepatocellular carcinoma (HCC). Upregulated MCM10 expression correlated with adverse clinicopathological features and inferior survival prognosis. Silencing of MCM10 significantly diminished HCC cell proliferation and oncogenic potential. Furthermore, Cyclin D1 was modulated by MCM10, and the combined evaluation of MCM10 and cyclin D1 showed superior prognostic performance in HCC patients. These findings underscore the synergistic value of the MCM10cyclin D1 molecular axis as a combined biomarker panel for prognostic prediction in HCC.
