Loss of UFL1 drives chromosome instability and tumorigenesis of prostate cancer

J Jimin Li (Department of Clinical Laboratory, Centre for Leading Medicine and Advanced Technologies of Institute of Health and Medicine, The First Affiliated Hospital of University of Science and Technology of China, Division of Life Sciences and Medicine, University of Science and Technology of China) F Fang Yang (State Key Laboratory of Inorganic Synthesis and Preparative Chemistry College of Chemistry) X Xiao Zhang L Liangfei Xu (Department of Clinical Laboratory, Centre for Leading Medicine and Advanced Technologies of Institute of Health and Medicine, The First Affiliated Hospital of University of Science and Technology of China, Division of Life Sciences and Medicine, University of Science and Technology of China) H Hui Zheng (Department of Clinical Laboratory, Centre for Leading Medicine and Advanced Technologies of Institute of Health and Medicine, The First Affiliated Hospital of University of Science and Technology of China, Division of Life Sciences and Medicine, University of Science and Technology of China) L Liu Liu (Shanghai Yuhui Pharmaceutical Technology (Group) Co., Ltd.) X Xin Wan (School of Materials Science and Engineering) T Tao Xu G Guanmin Jiang (Department of Clinical Laboratory, The Fifth Affiliated Hospital, Sun Yat-sen University) H Hao Wang (Division of Quantitative Sciences, Department of Oncology Johns Hopkins University School of Medicine Baltimore Maryland USA)

Abstract

Chromosomal instability (CIN) is a prevalent form of genomic instability in prostate cancer (PCa). However, its molecular mechanisms remain inadequately understood. This study demonstrates that reduced expression of UFM1-ligase 1 (UFL1) is commonly observed in PCa and correlates with elevated CIN rates. UFL1 deficiency results in severe mitotic defects, errors in chromosome segregation, and aneuploidy, thereby promoting malignant transformation. Mechanistically, UFL1 interacts with RNF20 and catalyzes its UFMylation, which enhances RNF20 binding to CEP192, facilitating its centrosomal localization and supporting mitotic spindle assembly. Additionally, downregulation of the microphthalmia-associated transcription factor (MITF) exacerbates PCa aggressiveness by suppressing UFL1 expression. These findings identify the MITF–UFL1–RNF20 axis as a critical regulator of spindle integrity and a potential therapeutic target in PCa.

Article Details

Volume / Issue Vol. 123, Issue 17
Published April 28, 2026
ISSN 0027-8424
Publisher National Academy of Sciences

Authors (10)

J

Jimin Li

Department of Clinical Laboratory, Centre for Leading Medicine and Advanced Technologies of Institute of Health and Medicine, The First Affiliated Hospital of University of Science and Technology of China, Division of Life Sciences and Medicine, University of Science and Technology of China

F

Fang Yang

State Key Laboratory of Inorganic Synthesis and Preparative Chemistry College of Chemistry

X

Xiao Zhang

L

Liangfei Xu

Department of Clinical Laboratory, Centre for Leading Medicine and Advanced Technologies of Institute of Health and Medicine, The First Affiliated Hospital of University of Science and Technology of China, Division of Life Sciences and Medicine, University of Science and Technology of China

H

Hui Zheng

Department of Clinical Laboratory, Centre for Leading Medicine and Advanced Technologies of Institute of Health and Medicine, The First Affiliated Hospital of University of Science and Technology of China, Division of Life Sciences and Medicine, University of Science and Technology of China

L

Liu Liu

Shanghai Yuhui Pharmaceutical Technology (Group) Co., Ltd.

X

Xin Wan

School of Materials Science and Engineering

T

Tao Xu

G

Guanmin Jiang

Department of Clinical Laboratory, The Fifth Affiliated Hospital, Sun Yat-sen University

H

Hao Wang

Division of Quantitative Sciences, Department of Oncology Johns Hopkins University School of Medicine Baltimore Maryland USA