ArticleCarcinogenesis2008
Plant flavonoid apigenin inactivates Akt to trigger apoptosis in human prostate cancer: an in vitro and in vivo study.
Article in Carcinogenesis, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 106 citations in OpenAlex.
- Stingless bee propolis: a comprehensive review of chemical constituents and health efficacy.Natural products and bioprospecting · 2025Review
- Metabolomic Characterization and Bioinformatic Studies of Bioactive Compounds in Two Varieties ofInternational journal of molecular sciences · 2025Article
- Effects of propolis intake on endurance exercise and molecular signaling related to inflammation and oxidative stress.Frontiers in nutrition · 2025Review
- Pharmacodynamics and safety in relation to dose and response of plant flavonoids in treatment of cancers.Inflammopharmacology · 2025Review
- Potential anticancer effects and toxicity of flavones luteolin and apigeninJournal of environmental science and health. Part C, Toxicology and carcinogenesis · 2025Review
- Computational investigation of the functional landscape of the protective role that extra virgin olive oil consumption may have on chronic lymphocytic leukemia.Journal of translational medicine · 2024Article
- The Pros and Cons of Estrogens in Prostate Cancer: An Update with a Focus on Phytoestrogens.Biomedicines · 2024Review
- Apigenin: Molecular Mechanisms and Therapeutic Potential against Cancer Spreading.International journal of molecular sciences · 2024Review
- Unlocking Potentially Therapeutic Phytochemicals in Capadulla (Metabolites · 2023Article
- An Update on the Therapeutic Anticancer Potential ofMolecules (Basel, Switzerland) · 2023Review
- The Potential Role of Apigenin in Cancer Prevention and Treatment.Molecules (Basel, Switzerland) · 2022Review
- Role of Induced Programmed Cell Death in the Chemopreventive Potential of Apigenin.International journal of molecular sciences · 2022Review
- TAB2 Promotes the Biological Functions of Head and Neck Squamous Cell Carcinoma Cells via EMT and PI3K Pathway.Disease markers · 2022Article
- Apigenin induces oxidative stress in mouse Sertoli TM4 cells.Veterinary world · 2021Article
- Apigenin Inhibits the Growth of Hepatocellular Carcinoma Cells by Affecting the Expression of microRNA Transcriptome.Frontiers in oncology · 2021Article
- Prostate cancer: Therapeutic prospect with herbal medicine.Current research in pharmacology and drug discovery · 2021Review
- Apigenin induces apoptosis by regulating Akt and MAPK pathways in human melanoma cell A375SM.Molecular medicine reports · 2020Article
- Review
- Apigenin as Tumor Suppressor in Cancers: Biotherapeutic Activity, Nanodelivery, and Mechanisms With Emphasis on Pancreatic Cancer.Frontiers in chemistry · 2020Review
- Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Inappropriate activation of phosphatidylinositol 3-kinase-Akt signaling contributes to the development of several human malignancies. Modulation of Akt activity is a strategy that may be valuable in chemopreventive and chemotherapeutic regimens. We have previously demonstrated that apigenin, a plant flavone, causes decreased survival in human prostate cancer cells. However, the molecular mechanism underlying this observation remains elusive. In the present study, we investigated the mechanisms of apigenin action on human prostate cancer PC-3 cells, which possess constitutively active Akt. Treatment of PC-3 cells with apigenin (5-40 microM) resulted in significant dose- and time-dependent decrease in Akt phosphorylation at Serine473. Apigenin-mediated dephosphorylation of Akt resulted in inhibition of its kinase activity, which was confirmed by reduced phosphorylation of proapoptotic proteins BAD and glycogen synthase kinase-3, essential downstream targets of Akt. Hypophosphorylation of BAD resulted in reduced interaction with 14-3-3beta protein after 20 microM apigenin exposure to PC-3 cells for 24 h. Inactivation of Akt seems to be associated with downregulation of insulin-like growth factor receptor 1 protein level and inhibition of its autophosphorylation upon apigenin treatment. Exposure to apigenin significantly induced caspase-9 activity and decreased the survival of PC-3 cells in a dose-dependent manner. Furthermore, Serine473 phosphorylation of ectopically expressed Akt in DU145 cells was significantly reduced upon 20 microM apigenin treatment. In vivo, apigenin intake through gavage resulted in inactivation of Akt and induction of apoptosis in PC-3 tumors. These results suggest that Akt inactivation and dephosphorylation of BAD is a critical event, at least in part, in apigenin-induced decreased cell survival and apoptosis.
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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.