| ISSN |
1007-9327 (print) and 2219-2840 (online) |
| 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/ |
| Copyright |
© The Author(s) 2025. Published by Baishideng Publishing Group Inc. All rights reserved. |
| Article Reprints |
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| Permissions |
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| Publisher |
Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA |
| Website |
http://www.wjgnet.com |
| Category |
Gastroenterology & Hepatology |
| Manuscript Type |
Basic Study |
| Article Title |
B cell CLL/lymphoma 10 promotes colorectal cancer cell proliferation and regulates cuproptosis sensitivity through the NF-κB signaling pathway
|
| Manuscript Source |
Unsolicited Manuscript |
| All Author List |
Peng-Tuo Xiao, Chang-Feng Li, Yuan-Da Liu, Jing Zhong, Xi-Lun Cui, Chang Liu and Wei Yang |
| ORCID |
|
| Funding Agency and Grant Number |
| Funding Agency |
Grant Number |
| National Natural Science Foundation of China |
82073299 |
| Special Project for Health Research Talents of Jilin Province |
2023SCZ25 |
|
| Corresponding Author |
Chang-Feng Li, Chief Physician, Postdoc, Professor, Department of Endoscopy Center, China-Japan Union Hospital of Jilin University, No. 126 Xiantai Street, Changchun 130000, Jilin Province, China. cfli@jlu.edu.cn |
| Key Words |
Colorectal cancer; Nuclear factor kappa-B; Cuproptosis; B cell CLL/lymphoma 10; Cell death |
| Core Tip |
B cell CLL/lymphoma 10 (BCL10) drives colorectal cancer (CRC) progression by promoting tumor cell proliferation, migration, and invasion, correlating with poor prognosis. It modulates CRC sensitivity to copper-induced cell death (cuproptosis), with overexpression increasing resistance and knockdown enhancing susceptibility. BCL10 activates nuclear factor kappa-B (NF-κB), suppressing DLAT-a key cuproptosis mediator. BCL10 knockdown increases DLAT oligomerization, boosting cuproptosis, while overexpression protects cells. Targeting BCL10 or the NF-κB-DLAT axis may improve CRC treatment by enhancing cuproptosis sensitivity. In vivo studies show BCL10 knockdown improves tumor response to copper therapy, supporting its therapeutic potential. These findings reveal BCL10 as a key CRC regulator, offering new treatment strategies. |
| Publish Date |
2025-09-05 06:36 |
| Citation |
<p>Xiao PT, Li CF, Liu YD, Zhong J, Cui XL, Liu C, Yang W. B cell CLL/lymphoma 10 promotes colorectal cancer cell proliferation and regulates cuproptosis sensitivity through the NF-κB signaling pathway. <i>World J Gastroenterol</i> 2025; 31(34): 109825</p> |
| URL |
https://www.wjgnet.com/1007-9327/full/v31/i34/109825.htm |
| DOI |
https://dx.doi.org/10.3748/wjg.v31.i34.109825 |
