ArticleVeterinary world2025
Annonacin induces apoptosis and modulates programmed death-ligand 1 and interferon-gamma expression in triple-negative breast cancer: Integrated
Article in Veterinary world, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
The trial behind it
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Who cites it
1 citing paper in PubMed.
- African Medicinal Plants Targeting Triple-Negative Breast Cancer (TNBC): A Systematic Review of Ethnobotanical Surveys, Phytochemistry and Anti-TNBC Studies.Pharmaceuticals (Basel, Switzerland) · 2026Review
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background and Aim: Triple-negative breast cancer (TNBC) presents therapeutic challenges due to its aggressive nature and lack of targeted treatments. Programmed death-ligand 1 (PD-L1) and interferon-gamma (IFN-γ) are key immune modulators in tumor immune evasion. Annonacin, a natural acetogenin from Annona species, has shown promising anticancer properties, though its immunomodulatory mechanisms remain underexplored. This study aimed to investigate the dual apoptotic and immunomodulatory effects of annonacin on PD-L1 and IFN-γ expression using combined molecular docking and Materials and Methods: Molecular docking simulations were conducted to assess annonacin's interaction with PD-L1 (Protein Data Bank [PDB] ID: 6PV9) and IFN-γ (PDB ID: 1FG9). Results: Docking scores indicated moderate binding affinities of annonacin to IFN-γ (-5.2 kcal/mol) and PD-L1 (-5.0 kcal/mol), involving both hydrogen bonds and hydrophobic interactions. Annonacin exhibited a selective cytotoxic effect on 4T1 cells with a half-maximal inhibitory concentration of 15 μg/mL and a selectivity index of 2.6. Apoptosis was induced in a concentration-dependent manner, with late apoptotic populations peaking at 25 μg/mL. PD-L1 and IFN-γ expression peaked at 6.25 μg/mL, followed by a decline at higher doses, suggesting a dose-dependent immunomodulatory shift from immune activation to suppression. Conclusion: Annonacin modulates immune checkpoint (PD-L1) and cytokine (IFN-γ) expression while promoting apoptosis in TNBC cells. These results highlight its potential as a dual-function anticancer agent, warranting further preclinical evaluation for use as a monotherapy or in combination with immunotherapies.
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