Targeting TRIM25 as a therapeutic strategy to enhance ferroptosis in glioblastoma cells
Our findings demonstrate that TRIM25 is a critical negative regulator of VDAC2-dependent ferroptosis in GBM. Targeting TRIM25 using the ANP<sub>SS</sub>(sgTRIM25) genome editing system effectively overcomes ferroptosis resistance and suppresses tumor growth, representing a viable therapeutic approach for GBM.
Authors
- S. Wang
- Mingrui Du
- Zhengcong Cao
- Qiang Hao (ORCID: https://orcid.org/0009-0002-4941-600X)
- Haozhe Qin (ORCID: https://orcid.org/0009-0006-4398-1525)
- Duo Yu
- Yuxin Wu (ORCID: https://orcid.org/0000-0003-4043-1617)
- Man Li (ORCID: https://orcid.org/0000-0002-4035-5266)
- Lin Wei (ORCID: https://orcid.org/0000-0002-3265-3554)
- Maorong Zhu
- Yingqi Zhang
- Wangqian Zhang
- Huihui Ou
- Guangzhao Yang
- Yalong He
- Yawen Wang
- Weidong Qin
- Dan Zheng
- Xiao Liu
- Jintao Gu
- Lei He
- Xiaolin Liu
- Kuo Zhang
- Cheng Zou
Institutions
- Northwestern Polytechnical University (CN)
- Air Force General Hospital PLA (CN)
- Central Hospital of Wuhan (CN)
- Command Hospital Air Force (IN)
- Xijing Hospital (CN)
- General Hospital of Central Theater Command
- Air Force Medical University (CN)
Publication Details
- Journal
- Journal of Nanobiotechnology
- Published
- 2026-01-07
- DOI
- https://doi.org/10.1186/s12951-025-03908-8
- Primary Topic
- Ferroptosis and cancer prognosis
- Type
- article
- Field-Weighted Citation Impact
- 0.00