Basic Study
Copyright ©The Author(s) 2024. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastrointest Oncol. Mar 15, 2024; 16(3): 1006-1018
Published online Mar 15, 2024. doi: 10.4251/wjgo.v16.i3.1006
Ubiquitin-specific protease 21 promotes tumorigenicity and stemness of colorectal cancer by deubiquitinating and stabilizing ZEB1
Jun-Jun Lin, Ye-Cai Lu
Jun-Jun Lin, Ye-Cai Lu, Department of Gastrointestinal Surgery, Chaohu Hospital of Anhui Medical University, Chaohu 238000, Anhui Province, China
Author contributions: Lin JJ wrote the manuscript; Lin JJ and Lu YC collected and analyzed the data; all authors read and approved the final manuscript.
Supported by Anhui Provincial Health Research Project, No. AHWJ2022c036.
Institutional review board statement: This study was approved by the Ethics Committee of Chaohu Hospital of Anhui Medical University (No. KYXM-2022-10-011).
Institutional animal care and use committee statement: The Animal Care and Use Committee of Beijing Viewsolid Biotechnology Co. LTD approved this work (No. VS2126A00153).
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Data sharing statement: All the data used to support the findings of this study are included within the article.
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: Ye-Cai Lu, MD, Professor, Department of Gastrointestinal Surgery, Chaohu Hospital of Anhui Medical University, No. 64 Chaohu North Road, Chaohu 238000, Anhui Province, China. 13965691202@163.com
Received: October 26, 2023
Peer-review started: October 26, 2023
First decision: December 31, 2023
Revised: January 4, 2024
Accepted: January 31, 2024
Article in press: January 31, 2024
Published online: March 15, 2024
Processing time: 138 Days and 1 Hours
ARTICLE HIGHLIGHTS
Research background

Previous studies have illustrated that ubiquitin-specific protease 21 (USP21) and ZEB1 has been confirmed to take part into the regulation of cancers’ progression through serving as a facilitator. However, the regulatory functions of USP21, and the relationship between USP21 and ZEB1 in colorectal cancer (CRC) progression need more investigations.

Research motivation

To search useful bio-targets for CRC prognosis and treatment.

Research objectives

In order to probe the regulatory functions and the relationship between USP21 and ZEB1 in CRC progression.

Research methods

The expressions of USP21 and ZEB1 in CRC were evaluated through real time-quantitative polymerase chain reaction (RT-qPCR) and western blot. The prognosis of GC patients with high or low USP21 (or ZEB1) expression was evaluated. The relationship between USP21 and ZEB1 in CRC progression was validated. The regulatory of USP21/ZEB1 axis in CRC progression was assessed via in vitro and in vivo experiments.

Research results

USP21 and ZEB1 exhibited higher expression in CRC, and resulted into poor prognosis. USP21 contributed to the stability of ZEB1 through modulating ubiquitination level. Furthermore, results revealed that USP21 strengthened cell proliferation, migration and stemness through regulating ZEB1.

Research conclusions

USP21 promoted tumorigenicity and stemness of CRC by deubiquitinating and stabilizing ZEB1.

Research perspectives

Other regulatory functions and related molecular mechanisms of USP21/ZEB1 axis in CRC progression may be investigated in the future, and its application in CRC treatment will be extended.