ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2024
Zosuquidar Promotes Antitumor Immunity by Inducing Autophagic Degradation of PD-L1.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed.
- Multistage responsive microneedle delivery system loaded oncolytic virus for topical therapy of melanoma.Acta pharmaceutica Sinica. B · 2026Article
- Targeting the Golgi apparatus enhances PD-L1 blockade and synergizes with oxaliplatin to improve immunotherapy efficacy.The Journal of biological chemistry · 2026Article
- Berberine induces PD-L1 degradation via the autophagy-lysosome pathway through the PI3K-Akt pathway and enhances immunogenic cell death in triple-negative breast cancer.Frontiers in immunology · 2026Article
- Review
- TBG096 Ameliorates Memory Deficiency in AD Mouse Model via Promoting Neurogenesis and Regulation of Hsc70/HK2/PKM2/LAMP2A Signaling Pathway.International journal of molecular sciences · 2025Article
- Autophagy in tumor immune escape and immunotherapy.Molecular cancer · 2025Review
- Zosuquidar Promotes Antitumor Immunity by Inducing Autophagic Degradation of PD-L1.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
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Authors and funding
12 authors.
Funding
Abstract
The intracellular distribution and transportation process are essential for maintaining PD-L1 (programmed death-ligand 1) expression, and intervening in this cellular process may provide promising therapeutic strategies. Here, through a cell-based high content screening, it is found that the ABCB1 (ATP binding cassette subfamily B member 1) modulator zosuquidar dramatically suppresses PD-L1 expression by triggering its autophagic degradation. Mechanistically, ABCB1 interacts with PD-L1 and impairs COP II-mediated PD-L1 transport from ER (endoplasmic reticulum) to Golgi apparatus. The treatment of zosuquidar enhances ABCB1-PD-L1 interaction and leads the ER retention of PD-L1, which is subsequently degraded in the SQSTM1-dependent selective autophagy pathway. In CT26 mouse model and a humanized xenograft mouse model, zosuquidar significantly suppresses tumor growth and accompanies by increased infiltration of cytotoxic T cells. In summary, this study indicates that ABCB1 serves as a negative regulator of PD-L1, and zosuquidar may act as a potential immunotherapy agent by triggering PD-L1 degradation in the early secretory pathway.
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Registered trials
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