<scp>PUF60</scp>‐Regulated Isoform Switching of <scp>MAZ</scp> Modulates Gastric Cancer Cell Migration
The prognostic difference of MAZ in GC stems from isoform-specific functional antagonism, with cell migration phenotypes governed by the MAZ-1/3 versus MAZ-2 ratio. Targeting MAZ alternative splicing, particularly via PUF60 modulation, represents a novel therapeutic strategy.
Authors
- Xian Shen (ORCID: https://orcid.org/0000-0003-3331-1676)
- Dong Xing (ORCID: https://orcid.org/0000-0003-3718-4539)
- Wanxia Cai (ORCID: https://orcid.org/0000-0002-2925-5846)
- Wangkai Xie
- Zhonghan Wu (ORCID: https://orcid.org/0009-0002-8875-7843)
- Ting C. Zhao (ORCID: https://orcid.org/0000-0003-1622-2663)
- Teming Zhang
- Tao Chen (ORCID: https://orcid.org/0000-0003-1306-6538)
- Zhiyuan Chen (ORCID: https://orcid.org/0000-0002-2482-4093)
- Zheng Han (ORCID: https://orcid.org/0000-0003-1537-3822)
- Jiaye Yu
- Xiangyang Xue (ORCID: https://orcid.org/0009-0008-3241-5282)
- Dan Xiang (ORCID: https://orcid.org/0000-0002-2379-1007)
- Dianfeng Mei
- Shiyu Feng (ORCID: https://orcid.org/0009-0003-5698-3253)
Institutions
- Wenzhou Medical University (CN)
- First Affiliated Hospital of Wenzhou Medical University (CN)
- Second Affiliated Hospital & Yuying Children's Hospital of Wenzhou Medical University (CN)
Publication Details
- Journal
- Cancer Medicine
- Published
- 2025-05-24
- DOI
- https://doi.org/10.1002/cam4.70977
- Citations
- 1
- Primary Topic
- Cancer-related gene regulation
- Type
- article
- Field-Weighted Citation Impact
- 0.81
Funders
- National Natural Science Foundation of China