ArticleFrontiers in pharmacology2022
Bafetinib Suppresses the Transcription of PD-L1 Through c-Myc in Lung
Article in Frontiers in pharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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
2 citing papers in PubMed.
- Alpha-Lipoic Acid Inhibits IFN-γ-Induced PD-L1 Expression in Prostate Cancer Cells and Enhances T-Cell-Mediated Anti-Tumor Cytotoxicity.Antioxidants (Basel, Switzerland) · 2026Article
- Regulatory mechanisms of PD-1/PD-L1 in cancers.Molecular cancer · 2024Review
Corrections and comments
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Authors and funding
6 authors.
Funding
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Abstract
Given the limitations of the existing antibody-based therapies, including immune-related adverse events, poor response rates, and intravenous route of dosing, small molecules inhibitors targeting PD-L1 are highly desirable. By cell-based screening, we found that tyrosine kinase inhibitor Bafetinib dramatically suppresses PD-L1 protein expression in a dose-dependent manner. In parallel, cell membrane PD-L1 is also reduced by Bafetinib. We confirm that Bafetinib doesn't affect the protein half-life of PD-L1 but significantly inhibits the transcription of PD-L1. Among the transcription factors that regulate PD-L1 expression, c-Myc is downregulated by Bafetinib. Bafetinib caused PD-L1 inhibition is abolished when c-Myc is knocked-down. Further, we identified that Bafetinib reduced c-Myc expression because of transcription inhibition. By using the CT26 tumor model, we further confirm that Bafetinib suppressed PD-L1 expression
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