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

Xiangbo Chen; Changxin Chen; Rensong He; Yisen Huang; Yubin Wang

doi:10.1007/s10620-024-08414-9

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

Dig Dis Sci. 2024 Apr 15. doi: 10.1007/s10620-024-08414-9. Online ahead of print.

Authors

Xiangbo Chen¹, Changxin Chen¹, Rensong He¹, Yisen Huang², Yubin Wang³

Affiliations

¹ Endoscopy Center, Quanzhou First Hospital Affiliated to Fujian Medical University, No. 250 East Street, Licheng District, Quanzhou, 362000, Fujian, China.
² Department of Gastroenterology, Quanzhou First Hospital Affiliated to Fujian Medical University, No. 250 East Street, Licheng District, Quanzhou, 362000, Fujian, China.
³ Department of Gastroenterology, Quanzhou First Hospital Affiliated to Fujian Medical University, No. 250 East Street, Licheng District, Quanzhou, 362000, Fujian, China. yubinwang@fjmu.edu.cn.

PMID: 38622461
DOI: 10.1007/s10620-024-08414-9

Abstract

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.

Keywords: Colorectal cancer; NF-κB; Proliferation; Tumorigenesis; UBXN11.