USP5 motivates immunosuppressive microenvironment in multiple myeloma by activating STAT2-PFKFB4-mediated glycolysis
These findings elucidated that USP5 served as a regulator of glycolysis-lactate to stimulate M2-like macrophage formation by regulating STAT2-PFKFB4 signaling, which supported that USP5 could be a viable therapeutic target of MM treatment.
Authors
- Yongliang Zheng (ORCID: https://orcid.org/0000-0002-7688-9198)
- Qinglan Wang (ORCID: https://orcid.org/0000-0002-7629-5058)
- Yanru Liu (ORCID: https://orcid.org/0000-0002-1367-8481)
- Shifeng Long
- Jing Shao (ORCID: https://orcid.org/0000-0001-7573-9326)
- Ting Ding (ORCID: https://orcid.org/0000-0002-6953-6853)
Institutions
- Jinggangshan University (CN)
Publication Details
- Journal
- Cancer Immunology Immunotherapy
- Published
- 2025-04-24
- DOI
- https://doi.org/10.1007/s00262-025-04031-1
- Citations
- 7
- Primary Topic
- Multiple Myeloma Research and Treatments
- Type
- article
- Field-Weighted Citation Impact
- 12.39