Basic Study
Copyright ©The Author(s) 2024. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. May 21, 2024; 30(19): 2564-2574
Published online May 21, 2024. doi: 10.3748/wjg.v30.i19.2564
Cell division cyclin 25C knockdown inhibits hepatocellular carcinoma development by inducing endoplasmic reticulum stress
Yan-Fei Li, Fang-Yuan Zheng, Xin-Yu Miao, Hai-Long Liu, Yao-Yao Zhang, Nai-Xia Chao, Fa-Rong Mo
Yan-Fei Li, Fang-Yuan Zheng, Xin-Yu Miao, Hai-Long Liu, Yao-Yao Zhang, Nai-Xia Chao, Fa-Rong Mo, School of Basic Medical Sciences, Guangxi Medical University, Nanning 530021, Guangxi Zhuang Autonomous Region, China
Nai-Xia Chao, Key Laboratory of Biological Molecular Medicine Research (Guangxi Medical University), Education Department of Guangxi Zhuang Autonomous Region, Nanning 530021, Guangxi Zhuang Autonomous Region, China
Fa-Rong Mo, Key Laboratory of Human Development and Disease Research (Guangxi Medical University), Education Department of Guangxi Zhuang Autonomous Region, Nanning 530021, Guangxi Zhuang Autonomous Region, China
Co-first authors: Yan-Fei Li and Fang-Yuan Zheng.
Co-corresponding authors: Fa-Rong Mo and Nai-Xia Chao.
Author contributions: Li YF, Zheng FY, Miao XY, Liu HL, Zhang YY performed research. All authors contributed to the manuscript review. Li YF and Zheng FY contributed equally to this work as co-first authors. Because they made equal and significant contributions throughout the research process, such as research design, acquisition of data, statistical analysis, creation and improvement of tables and figures, and drafting of the manuscript. Mo FR and Chao NX are designated as co-corresponding authors in recognition of their roles as supervisors in the project. Mo FR was the project leader responsible for funding acquisition for this study. He mainly contributed to research design, supervision of the project, providing material support, and handling the submission and revision of the manuscript during this study. Chao NX focused on project administration tasks such as technical support for establishing a xenograft mouse model with CDC25C knockdown, enhancing the tables and figures, conducting data statistical analysis, and participating in manuscript revisions. Mo FR and Chao NX made equal contributions in terms of technical and material support, research design, study supervision, manuscript submission, and revision.
Supported by Natural Science Foundation of Guangxi Zhuang Autonomous Region, China, No. 2023GXNSFAA026070 and No. 2018GXNSFAA281071.
Institutional animal care and use committee statement: All animal experiments were reviewed and approved by the Ethics Review Committee for Animal Experiments at Guangxi Medical University (Approval Number: 202201093).
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Data sharing statement: No additional data are available.
ARRIVE guidelines statement: The authors have read the ARRIVE guidelines, and the manuscript was prepared and revised according to the ARRIVE guidelines.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Fa-Rong Mo, MD, Professor, School of Basic Medical Sciences, Guangxi Medical University, No. 22 Shuangyong Road, Nanning 530021, Guangxi Zhuang Autonomous Region, China. farongmo@126.com
Received: January 30, 2024
Revised: April 5, 2024
Accepted: April 18, 2024
Published online: May 21, 2024
Processing time: 110 Days and 22.6 Hours
Core Tip

Core Tip: In the current study, cell division cyclin 25C (CDC25C) is an important cell cycle regulatory protein and a potential target for cancer treatment. CDC25C knockdown not only inhibited cell proliferation and migration but also significantly increased the endoplasmic reticulum (ER) stress response. Furthermore, CDC25C knockdown promoted ER stress-induced apoptosis in hepatocellular carcinoma (HCC) cells. The regulatory mechanism of CDC25C in HCC development might be related to the activation of ER stress and the ER stress-induced apoptosis signaling pathway.