UBXN11 Predicts as a Poor Index for Colorectal Cancer and Contributes to the Tumorigenesis by Activating NF-κB Signaling

• Published in: Digestive diseases and sciences 2024-06, Vol.69 (6), p.2074-2082
• Main Authors: Chen, Xiangbo, Chen, Changxin, He, Rensong, Huang, Yisen, Wang, Yubin
• Format: Article
• Language: English
• Subjects: Biochemistry; Colorectal cancer; Esophageal cancer; Gastroenterology; Hepatology; Medicine; Medicine & Public Health; Oncology; Original Article; Transplant Surgery; Tumorigenesis
• ISSN: 0163-2116; 1573-2568; 1573-2568
• DOI: 10.1007/s10620-024-08414-9

Background The complex mechanisms of colorectal cancer (CRC) pathogenesis and progression remain poorly understood. This study endeavors to unravel the role of UBXN11within the context of CRC. Methods UBXN11 expression level in CRC, stomach adenocarcinoma and esophageal carcinoma, and the overall survival in corresponding cancers were analyzed using UALCAN database. Human CRC cell lines and xenograft mouse model with UBXN11 overexpression were established to investigate the pathological role of UBXN11 in CRC progression. Luciferase assay, qPCR, and Western blot were performed to dissect the interaction between UBXN11 and NF-κB signaling. Results Heightened UBXN11 expression was observed in various digestive tract tumors, which was positively correlated with the reduced overall survival rates in CRC patients. Overexpression of UBXN11 significantly enhanced CRC cell proliferation in vitro and promoted tumor growth in vivo. Mechanistically, UBXN11 promoted CRC tumorigenesis through increasing the activation of NF-κB signaling pathway. Conclusions This study underscores the pivotal role of UBXN11 in CRC progression and paves the way for novel therapeutic strategies for CRC treatment.