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©The Author(s) 2025. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Mar 14, 2025; 31(10): 103133
Published online Mar 14, 2025. doi: 10.3748/wjg.v31.i10.103133
Published online Mar 14, 2025. doi: 10.3748/wjg.v31.i10.103133
SEL1L-mediated endoplasmic reticulum associated degradation inhibition suppresses proliferation and migration in Huh7 hepatocellular carcinoma cells
Jia-Nan Chen, Zhong-Yang Shen, School of Medicine, Nankai University, Tianjin 300071, China
Jia-Nan Chen, Zhong-Yang Shen, Department of Organ Transplant, Tianjin First Central Hospital, School of Medicine, Nankai University, Tianjin 300192, China
Li Wang, Yu-Xin He, Xiao-Wei Sun, Long-Jiao Cheng, Ya-Nan Li, Sei Yoshida, State Key Laboratory of Medicinal Chemical Biology, College of Life Sciences, Frontiers Science Center for Cell Responses, Nankai University, Tianjin 300071, China
Sei Yoshida, Zhong-Yang Shen, Research Institute of Transplant Medicine, Nankai University, Tianjin 300192, China
Sei Yoshida, Nankai International Advanced Research Institute, Shenzhen 518045, Guangdong Province, China
Zhong-Yang Shen, Tianjin Key Laboratory for Organ Transplantation, Tianjin First Central Hospital, School of Medicine, Nankai University, Tianjin 300192, China
Co-corresponding authors: Sei Yoshida and Zhong-Yang Shen.
Author contributions: Chen JN, Wang L, He YX, Sun XW, Cheng LJ and Li YN performed the research; Chen JN and Wang L analyzed the data; Yoshida Sei and Shen ZY designed the study; All authors have read and approved the final manuscript.
Supported by the National Natural Science Foundation of China, No. 82241219, No. 82127808 and No. 81921004; and The Shenzhen Science and Technology Program, No. JCYJ20210324120813037.
Institutional review board statement: This study does not involve any human experiments.
Institutional animal care and use committee statement: Our research obtained ethical approval from the Ethics committee at Nankai University (approval No. 2025-SYDWLL-000002).
Conflict-of-interest statement: The authors declare that they have no 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: 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: Zhong-Yang Shen, MD, Professor, School of Medicine, Nankai University, No. 94 Fukang Road, Nankai District, Tianjin 300071, China.
Received: November 11, 2024
Revised: January 4, 2025
Accepted: February 5, 2025
Published online: March 14, 2025
Processing time: 107 Days and 22.3 Hours
Revised: January 4, 2025
Accepted: February 5, 2025
Published online: March 14, 2025
Processing time: 107 Days and 22.3 Hours
Core Tip
Core Tip: The endoplasmic reticulum-associated degradation (ERAD) inhibitor suppressed cell proliferation and migration and promoted apoptosis. SEL1L-HRD1 significantly influenced Huh7 cell growth. SEL1L knockout suppressed tumor cell proliferation and migration, and enhanced apoptosis. Mass spectrometry revealed EXT2 is a primary substrate of ERAD. SEL1L knockout significantly increased the protein expression of EXT2, whereas EXT2 knockdown partially restored the effect of SEL1L knockout. In conclusion, this study showed the function and possible mechanisms of ERAD in hepatocellular carcinoma, providing new insights into more effective treatment and strategies for liver cancer.