KIF26B promotes bladder cancer progression through activating the NF-κB signaling pathway.

Authors

Dan-Ni Chen, Jia-Ming Wang, Feng-Hao Zhang, Hong-Ying Ye, Yi-Ru Chen, Feng Zhao, Xiao Wang

Published in

iScience. Volume 29. Issue 7. Pages 116577. Jul 17, 2026. Epub Jul 02, 2026.

Abstract

Kinesin superfamily plays pivotal role in tumor progression. Our previous study identified KIF26B as a novel biomarker for bladder cancer diagnosis and prognosis. Herein, we illustrated another role of KIF26B in bladder cancer progression through stimulating the NF-κB signaling pathway. Mechanically, KIF26B activated the NF-κB signaling pathway by enabling nuclear localization of NF-κB subunit p65 without influencing its protein stability. Instead, KIF26B could recruit TRIM21 and add K63-linked ubiquitin to p65, which allowed its nuclear localization. Further, PKCε responded to TNFα and mediated the phosphorylation of KIF26B at the S592 site, further increasing the interaction between KIF26B and p65. In turn, the activated NF-κB signaling pathway elevated the transcription of kif26b and her2, forming a KIF26B/NF-κB positive feedback loop and further promoting bladder cancer progression. Combining radiation and KIF26B blockage therapy yielded better anti-tumor effects.

PMID:
42436976
Bibliographic data and abstract were imported from PubMed on 12 Jul 2026.

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