ArticleFood & nutrition research2024
Inhibition of triple-negative breast cancer growth via delphinidin-mediated suppression of the JAK2/STAT3/PD-L1 pathway.
Article in Food & nutrition research, 2024. 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.
- JAK/STAT-mediated regulation of PD-L1 expression in breast cancer: Molecular mechanisms and implications for immunotherapy.iScience · 2026Review
- Targeting cancer with delphinidin: from molecular insights to therapeutic implications.Frontiers in pharmacology · 2026Review
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Breast cancer is a leading cause of cancer-related mortality among women globally, with triple-negative breast cancer (TNBC) being particularly aggressive. Delphinidin (Dp), an anthocyanin monomer, has shown promising health benefits. Objective: This study investigates the effects of Dp on TNBC and aims to elucidate its specific mechanisms of action. Design: We utilized cell counting kit-8 (CCK-8) assays, colony formation assays, and scratch assays to evaluate the influence of Dp on the proliferation and migration of TNBC cells. Flow cytometry was employed to analyze programmed cell death-ligand 1 (PD-L1) and Cluster of Differentiation 69 expression, while Western blotting assessed the levels of PD-L1, Janus Kinase 2 (JAK2), Signal Transducer and Activator of Transcription 3 (STAT3), p-JAK2, p-STAT3, and exosomal marker proteins. Additionally, enzyme-linked immunosorbent assay (ELISA) was conducted to measure concentrations of PD-L1, interferon-γ (IFN-γ), and tumor necrosis factor-β (TNF-β). Results: Dp effectively inhibited TNBC cell proliferation and migration, as evidenced by CCK-8, colony formation, and scratch assays. Flow cytometry and Western blot analysis indicated a reduction in PD-L1 expression in TNBC cells. Meanwhile, we successfully isolated TNBC cell-derived exosomes, with ELISA experiments showing a decrease in PD-L1 expression in these exosomes following Dp treatment. In a co-culture system with TNBC and Jurkat cells, Dp enhanced Cluster of Differentiation 69 expression and reactivated Jurkat cells, resulting in increased secretion of IFN-γ and TNF-β. Additionally, Dp significantly reduced the p-JAK2/JAK2 and p-STAT3/STAT3 ratios in TNBC cells. Conclusion: Dp may exert its anti-TNBC effects by downregulating PD-L1 expression in TNBC cells and exosomes through the JAK2/STAT3 signaling pathway, potentially restoring T cell activity and modifying the tumor microenvironment.
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