ArticleCell death discovery2018
Apigenin suppresses the stem cell-like properties of triple-negative breast cancer cells by inhibiting YAP/TAZ activity.
Article in Cell death discovery, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 2 of them syntheses that pooled it.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
64 citing papers in PubMed, 2 syntheses or guidelines pooled it, 117 citations in OpenAlex.
- Therapy-resistant breast cancer in focus: Clinically relevant mitigation by flavonoids targeting cancer stem cells.Frontiers in pharmacology · 2023Pooled it
- Signaling Pathways and Natural Compounds in Triple-Negative Breast Cancer Cell Line.Molecules (Basel, Switzerland) · 2022Pooled it
- Metabolomics-Driven Bioactivity-Guided Isolation and Molecular Docking Reveal Antibreast Cancer Metabolome Heterogeneity in Polygonum spp.Biomedical chromatography : BMC · 2026Article
- Hippo pathway at the crossroads of stemness and therapeutic resistance in breast cancer.Molecular oncology · 2026Review
- Targeting TYRO3 attenuates apoptotic cell-driven cancer stemness in triple negative breast cancer.Cell communication and signaling : CCS · 2026Article
- Review
- Targeting Key Molecular Mechanisms in Triple-Negative Breast Cancer Therapies with Natural Compounds.Current pharmaceutical design · 2026Review
- Cancer chemoprevention: signaling pathways and strategic approaches.Signal transduction and targeted therapy · 2025Review
- Molecular Mechanisms of Dietary Compounds in Cancer Stem Cells from Solid Tumors: Insights into Colorectal, Breast, and Prostate Cancer.International journal of molecular sciences · 2025Review
- Unraveling the Hippo pathway: YAP/TAZ as central players in cancer metastasis and drug resistance.EXCLI journal · 2025Review
- Targeting Hippo-YAP/TAZ signaling pathway: an updated review demonstrating the therapeutic potential of key plant derived anticancer compounds.Frontiers in pharmacology · 2025Review
- Apigenin promotes melanogenesis and melanosome transport through the c-KIT/Raf-1/MAPK/CREB pathway in HEMCs.Frontiers in pharmacology · 2025Article
- Modulating versatile pathways using a cleavable PEG shell and EGFR-targeted nanoparticles to deliver CRISPR-Cas9 and docetaxel for triple-negative breast cancer inhibition.Archives of pharmacal research · 2024Article
- Naturally Occurring Phytochemicals to Target Breast Cancer Cell Signaling.Applied biochemistry and biotechnology · 2024Review
- Article
- The PML1-WDR5 axis regulates H3K4me3 marks and promotes stemness of estrogen receptor-positive breast cancer.Cell death and differentiation · 2024Article
- Apigenin: Molecular Mechanisms and Therapeutic Potential against Cancer Spreading.International journal of molecular sciences · 2024Review
- Apigenin and its combination with Vorinostat induces apoptotic-mediated cell death in TNBC by modulating the epigenetic and apoptotic regulators and related miRNAs.Scientific reports · 2024Article
- Targeting Cervical Cancer Stem Cells by Phytochemicals.Current medicinal chemistry · 2024Review
- Mechanism of Apigenin against breast cancer stem cells: network pharmacology and experimental validation.Frontiers in pharmacology · 2024Article
4 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Triple-negative breast cancer (TNBC) remains a clinical challenge because of the absence of effective therapeutic targets. In TNBC, overexpression of YAP and TAZ correlates with bioactivities of cancer stem cells (CSCs), high histological grade, resistance to chemotherapy, and metastasis. Thus, YAP/TAZ may serve as potential therapeutic targets in TNBC. To identify YAP/TAZ inhibitors, in previous experiments, we screened a library of natural compounds by using YAP/TAZ luciferase reporter assay and identified apigenin as a potential inhibitor. In this study, we demonstrated that apigenin significantly suppressed the proliferation and migration of TNBC cells. Furthermore, we demonstrated that apigenin inhibited stemness features of TNBC cells in both in vitro and in vivo assays. Our mechanism study demonstrated that apigenin decreased YAP/TAZ activity and the expression of target genes, such as CTGF and CYR61, in TNBC cells. We also showed that apigenin disrupted the YAP/TAZ-TEADs protein-protein interaction and decreased expression of TAZ sensitized TNBC cells to apigenin treatment. Collectively, our studies suggest that apigenin is a promising therapeutic agent for the treatment of TNBC patients with high YAP/TAZ activity.
Identifiers
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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.