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Updated: Jan 8, 2026

3-D Cell Culture System for Studying Invasion and Evaluating Therapeutics in Bladder Cancer

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Published on: September 13, 2018

Expresión aberrante de KIF26B promueve la progresión del cáncer de vejiga al impulsar la localización nuclear de

Jia-Ming Wang¹, Hai-Yun Xie², Feng-Hao Zhang¹

¹Department of Urology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, People's Republic of China.

Journal of hematology & oncology

|December 21, 2025

Abstract:

Abnormal expression of kinesins has been observed in several types of cancer. The present study provided the first evidence that KIF26B could induce RNA m⁵C modification in bladder cancer (BCa). Detailly, KIF26B interacted with NSUN2 and recruited ubiquitinase STUB1 to promote K63-linked ubiquitination of NSUN2 at K511 site. K63-linked ubiquitination enabled NSUN2 to bind to KPNA1 and translocate into nucleus where it drove RNA m⁵C modification. Furthermore, KIF26B induced liquid-liquid phase separation (LLPS) of YBX1 and upregulated IL-6 expression through NSUN2/m⁵C/YBX1 axis. Secreted IL-6 then activated STAT3 signaling to promote transcription of kif26b through direct binding between STAT3 and kif26b promoter. IL-6 also recruited DLAT to acetylate NSUN2 at K229 site and increased association affinity between NSUN2 and KIF26B. Together, these established a KIF26B/NSUN2/m⁵C/IL-6 positive feedback loop, suggesting that targeting KIF26B may be a promising therapeutic strategy for BCa.

Palabras clave:

Cáncer de vejiga KIF26B m5C NSUN2 Modificación post-traduccional

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