ArticleDiscover oncology2025
ADAM9 drives PD-L1 shedding via IL-6 suppression and exploring therapeutic role of Bufalin treatment in hepatocellular carcinoma.
Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- ADAM9 in tumor biology: molecular functions, clinical implications, and therapeutic targeting.Cellular & molecular biology letters · 2026Review
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3 authors.
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Abstract
The treatment landscape for advanced hepatocellular carcinoma (HCC) has changed significantly with the recent introduction of immunotherapy, particularly immune checkpoint inhibitors (ICIs), such as those for programmed cell death ligand 1 (PD-L1). However, the heterogeneous response to ICIs is still high, which may be related to different tumor microenvironment (TME) influenced by inflammatory cytokines like IL6. High expression of ADAM9 a type I transmembrane proteinases can affect tumor progression by cleaving various cell surface proteins PD-L1, and alter TME. Bufalin (BUF) a traditional Chinese medicine with important anti-cancer and anti-inflammation property has found to stimulates anti-tumor immune response by modulating TME, and enhances ICIs antitumor activity. In this study we first show the correlation between ADAM9 and HCC patient clinical outcomes and evaluate the stimulating effect of IL6 on ADAM9 expression and its protease activity mediates PD-L1 shedding, and investigates the immune modulating function of BUF to increases anti-PD-1 efficiency by inhibiting sPD-L1 induction in HCC cell lines and treated animals. We discovered that IL6 treatment can highly stimulate ADAM9 expression and its PD-L1 shedding activity, while BUF treatment down regulates ADAM9, and its protease activity by attenuating IL6. In conclusion BUF treatment can be considered as an adjuvant therapy lowering s PD-L1 formation to improve antitumor immunity and immunotherapy responses in HCC.
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