ZNF263–NuRD-mediated repression of STAT1 curtails MHC-I antigen presentation and IFN-γ efficacy in prostate cancer

H Han Guan (Department of Urology, Zhongda Hospital, School of Medicine, Southeast University) L Likai Mao (Department of Urology, Zhongda Hospital, School of Medicine, Southeast University) F Fang Fang T Tiange Wu (Department of Urology, Zhongda Hospital, School of Medicine, Southeast University) Y Yifei Cheng (Key Laboratory of Bio-inspired Materials and Interfacial Science, Technical Institute of Physics and Chemistry) Z Zonghao You (Department of Urology, Zhongda Hospital, School of Medicine, Southeast University) H Hao Lin R Ruixin Zhang (Department of Urology, Zhongda Hospital, School of Medicine, Southeast University) J Junyong Zhuang (Department of Urology, Zhongda Hospital, School of Medicine, Southeast University) G Gao-Jun Teng (Center of Interventional Radiology and Vascular Surgery, Department of Radiology, Zhongda Hospital, School of Medicine, Southeast University) C Chuanjun Shu (Department of Bioinformatics, School of Biomedical Engineering and Informatics, Nanjing Medical University) S Shenghong Ju (Nurturing Center of Jiangsu Province for State Laboratory of AI Imaging & Interventional Radiology, Department of Radiology, Zhongda Hospital, School of Medicine) M Ming Chen W Wenchao Li (Department of Urology, Zhongda Hospital, School of Medicine, Southeast University) B Bin Xu

Abstract

Loss of major histocompatibility complex (MHC)-I is a hallmark of prostate cancer (PCa) immune evasion and immunotherapy failure. Here, we identify ZNF263 as a transcriptional repressor that silences MHC-I by recruiting nucleosome-remodeling and deacetylase (NuRD) to the STAT1 promoter, reducing STAT1 and MHC-I expression. Hypoxia enhances this repression through two ZNF263 modifications: phosphorylation-driven phase separation that strengthens NuRD interaction and O-GlcNAcylation at S662 that aids STAT1 promoter binding. O-GlcNAcylation also promotes interaction with protein kinase, DNA‑activated catalytic subunit (PRKDC), amplifying phosphorylation. Interferon‑gamma (IFN‑γ)‑induced MHC-I induction is augmented upon ZNF263 loss. In silico docking identified Viroptic as a Krüppel‑associated box (KRAB) pocket binder disrupting ZNF263–NuRD, derepressing STAT1, and potentiating IFN-γ antitumor immunity in vivo. High ZNF263 correlates with low MHC-I, scarce CD8+ T cells, and poor survival, providing rationale for targeting ZNF263 in PCa immunotherapy.

Article Details

Volume / Issue Vol. 123, Issue 30
Published July 28, 2026
ISSN 0027-8424
Publisher National Academy of Sciences

Authors (15)

H

Han Guan

Department of Urology, Zhongda Hospital, School of Medicine, Southeast University

L

Likai Mao

Department of Urology, Zhongda Hospital, School of Medicine, Southeast University

F

Fang Fang

T

Tiange Wu

Department of Urology, Zhongda Hospital, School of Medicine, Southeast University

Y

Yifei Cheng

Key Laboratory of Bio-inspired Materials and Interfacial Science, Technical Institute of Physics and Chemistry

Z

Zonghao You

Department of Urology, Zhongda Hospital, School of Medicine, Southeast University

H

Hao Lin

R

Ruixin Zhang

Department of Urology, Zhongda Hospital, School of Medicine, Southeast University

J

Junyong Zhuang

Department of Urology, Zhongda Hospital, School of Medicine, Southeast University

G

Gao-Jun Teng

Center of Interventional Radiology and Vascular Surgery, Department of Radiology, Zhongda Hospital, School of Medicine, Southeast University

C

Chuanjun Shu

Department of Bioinformatics, School of Biomedical Engineering and Informatics, Nanjing Medical University

S

Shenghong Ju

Nurturing Center of Jiangsu Province for State Laboratory of AI Imaging & Interventional Radiology, Department of Radiology, Zhongda Hospital, School of Medicine

M

Ming Chen

W

Wenchao Li

Department of Urology, Zhongda Hospital, School of Medicine, Southeast University

B

Bin Xu