ArticleFrontiers in pharmacology2024
Mechanism of Apigenin against breast cancer stem cells: network pharmacology and experimental validation.
Article in Frontiers in pharmacology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- 4-Methylumbelliferone for type 1 diabetes therapy: evidence for β-cell protection via EGFR/PI3K/Akt signaling.Journal of endocrinological investigation · 2026Article
- Comparative Evaluation of the Cytotoxic Effect of Dysphania ambrosioides Extracts Against Human Breast and Cervical Cancer Cells.Chemistry & biodiversity · 2026Article
- Phytochemical Composition and Biological Activities ofPlants (Basel, Switzerland) · 2026Review
- Unveiling the anti-cancer properties of apigenin via targeting different molecular signatures: A Review.Molecular biology reports · 2026Review
- Apigenin as a Multi-Targeted Agent in Gastrointestinal Cancers: A Systems Pharmacology Approach.Advanced pharmaceutical bulletin · 2026Article
- Integrated in silico and in vitro evaluation of Genistein and Apigenin as dual inhibitors of PARP1 and ESR1 in breast cancer.BMC pharmacology & toxicology · 2026Article
- Exploring the pharmacokinetics, drug-likeness, and toxicological features of anticancer flavonoids: a Boulevard to explore their clinical translational potential.Frontiers in pharmacology · 2025Review
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apigenin (API), a traditionally sourced flavonoid, is recognized for its anti-neoplastic properties. Despite well-documented effects on tumorigenesis, the detailed therapeutic impact on breast cancer stem cells (BCSCs) and the associated molecular mechanisms are yet to be clarified. The objective of this study is to elucidate the therapeutic effects of API on BCSCs and to uncover its molecular mechanisms through network pharmacology and experimental validation. Interactions of API with candidate targets were examined through target screening, enrichment analysis, construction of protein-protein interaction networks, and molecular docking. MCF-7-derived BCSCs were utilized as a model system to investigate and substantiate the anti-BCSC effects of API and the underlying mechanism. Molecular docking studies have shown that API and TP53 exhibit favorable binding affinity. Compared with the negative control group, API effectively suppressed the expression of BCSC-related proteins such as ALDH1A1, NANOG, EpCAM, and MYC, downregulated p-PI3K and p-AKT, and upregulated p53. This study demonstrates that API can play an anti-BCSC role by regulating the PI3K/AKT/p53 pathway in BCSCs of MCF-7 cells, highlighting its potential as a therapeutic agent for targeting BCSCs.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.