Basic Study
Copyright ©The Author(s) 2025. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastrointest Oncol. Jul 15, 2025; 17(7): 107971
Published online Jul 15, 2025. doi: 10.4251/wjgo.v17.i7.107971
SAC3 domain containing 1 intervention in energy metabolism reprogramming assists in the progression of hepatocellular carcinoma
Xue-Jing Lin, Er-Jiang Tang, Bin Sun, Ai-Li Wang, Ying Chen, Lei Chen, Yi-Yang Xue, A-Jian Li, Chun-Ying Liu
Xue-Jing Lin, Er-Jiang Tang, Bin Sun, Ai-Li Wang, Ying Chen, Lei Chen, Center for Clinical Research and Translational Medicine, Yangpu Hospital, Tongji University School of Medicine, Shanghai 200090, China
Xue-Jing Lin, Chun-Ying Liu, National Center for Liver Cancer, Naval Medical University, Shanghai 201805, China
Yi-Yang Xue, Department of Chemistry and Biochemistry, University of California, Santa Barbara, Santa Barbara, CA 93106, United States
A-Jian Li, Department of General Surgery, Yangpu Hospital, Tongji University School of Medicine, Shanghai 200090, China
Co-first authors: Xue-Jing Lin and Er-Jiang Tang.
Co-corresponding authors: A-Jian Li and Chun-Ying Liu.
Author contributions: Lin XJ, Li AJ, and Liu CY designed the experiments; Lin XJ and Tang EJ performed the experiments; Lin XJ, Tang EJ, and Sun B collected the data and analyzed the data; Wang AL, Chen Y, Chen L, and Xue YY performed support with experimental techniques and validated the data analysis; Li AJ and Liu CY contributed to the design, revision and study supervision; Lin XJ and Tang EJ made contributions in experimental implementation and data collection, they contributed equally to this article, they are the co-first authors of this manuscript; Li AJ and Liu CY contributed to the design, revision and funding of the research project, they contributed equally to this article, they are the co-corresponding authors of this manuscript; and all authors have read and approved the final manuscript.
Supported by the Shanghai Yangpu District Science and Technology Commission, No. YPQ202303; Shanghai Municipal Health Commission Clinical Research Special Project, No. 202240122; and Shanghai Medical Innovation Research Special Project, No. 22Y11908600.
Institutional animal care and use committee statement: All procedures involving animals were reviewed and approved by the Institutional Animal Care and Use Committee of Naval Medical University, PLA.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
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: No additional data are available.
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: Chun-Ying Liu, PhD, Associate Professor, National Center for Liver Cancer, Naval Medical University, No. 366 Qianjv Road, Shanghai 201805, China.cyliu@sibcb.ac.cn
Received: April 11, 2025
Revised: May 8, 2025
Accepted: June 19, 2025
Published online: July 15, 2025
Processing time: 104 Days and 3.3 Hours
Core Tip

Core Tip: The study revealed that the expression of SAC3 domain containing 1 (SAC3D1) was elevated in hepatocellular carcinoma and closely related to a poor prognosis. SAC3D1 facilitated the proliferation and migration of hepatocellular carcinoma cells in vitro and in vivo. The increase of SAC3D1 Leads to more β-Catenin accumulating in the nucleus, facilitating the expression of c-Myc, one of the upstream regulatory factors of glycolysis. The iCRT3, an antagonist of β-Catenin, could counteract the increase of c-Myc induced by SAC3D1, while also downregulating the expression of glycolysis-related proteins. In conclusion, SAC3D1 augmented glycolysis and adenosine triphosphate generation via β-Catenin/c-Myc axis.