ArticleFree radical biology & medicine2008
Apigenin-induced prostate cancer cell death is initiated by reactive oxygen species and p53 activation.
Article in Free radical biology & medicine, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
60 citing papers in PubMed, 1 synthesis or guideline pooled it, 153 citations in OpenAlex.
- Phytochemicals in Inhibition of Prostate Cancer: Evidence from Molecular Mechanisms Studies.Biomolecules · 2022Pooled it
- Apigenin as a Multi-Targeted Agent in Gastrointestinal Cancers: A Systems Pharmacology Approach.Advanced pharmaceutical bulletin · 2026Article
- Targeted elimination of CD44RSC advances · 2026Article
- Nano-phytochemical-based formulations as promising opportunities for prostate cancer therapy and management: a comprehensive narrative review.Medical oncology (Northwood, London, England) · 2025Review
- Therapeutic Potential of Plant- and Marine-Derived Bioactive Compounds in Prostate Cancer: Mechanistic Insights and Translational Applications.Pharmaceuticals (Basel, Switzerland) · 2025Review
- The Pros and Cons of Estrogens in Prostate Cancer: An Update with a Focus on Phytoestrogens.Biomedicines · 2024Review
- Polyphenolic Nanomedicine Regulating Mitochondria REDOX for Innovative Cancer Treatment.Pharmaceutics · 2024Review
- The Antioxidant Potential and Anticancer Activity ofAntioxidants (Basel, Switzerland) · 2024Article
- Apigenin: Molecular Mechanisms and Therapeutic Potential against Cancer Spreading.International journal of molecular sciences · 2024Review
- Modulating the p53-MDM2 pathway: the therapeutic potential of natural compounds in cancer treatment.EXCLI journal · 2024Review
- Molecular Insight into Prostate Cancer: Preventive Role of Selective Bioactive Molecules.Life (Basel, Switzerland) · 2023Review
- Phytochemical Constituents and Derivatives ofInternational journal of molecular sciences · 2023Review
- The mechanism of flavonoids fromFrontiers in pharmacology · 2023Article
- Review
- The Potential Role of Apigenin in Cancer Prevention and Treatment.Molecules (Basel, Switzerland) · 2022Review
- Anti-prostate cancer protection and therapy in the framework of predictive, preventive and personalised medicine - comprehensive effects of phytochemicals in primary, secondary and tertiary care.The EPMA journal · 2022Review
- Apigenin Targets MicroRNA-155, Enhances SHIP-1 Expression, and Augments Anti-Tumor Responses in Pancreatic Cancer.Cancers · 2022Article
- Role of Induced Programmed Cell Death in the Chemopreventive Potential of Apigenin.International journal of molecular sciences · 2022Review
- AnAnalytical cellular pathology (Amsterdam) · 2021Article
- Hypericin Enhances Paclitaxel-Induced B16-F10 Cell Apoptosis by Activating a CytochromeFrontiers in pharmacology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Apigenin, a plant flavone, potentially activates wild-type p53 and induces apoptosis in cancer cells. We conducted detailed studies to understand its mechanism of action. Exposure of human prostate cancer 22Rv1 cells, harboring wild-type p53, to growth-suppressive concentrations (10-80 microM) of apigenin resulted in the stabilization of p53 by phosphorylation on critical serine sites, p14ARF-mediated downregulation of MDM2 protein, inhibition of NF-kappaB/p65 transcriptional activity, and induction of p21/WAF-1 in a dose- and time-dependent manner. Apigenin at these doses resulted in ROS generation, which was accompanied by rapid glutathione depletion, disruption of mitochondrial membrane potential, cytosolic release of cytochrome c, and apoptosis. Interestingly, we observed accumulation of a p53 fraction to the mitochondria, which was rapid and occurred between 1 and 3 h after apigenin treatment. All these effects were significantly blocked by pretreatment of cells with the antioxidant N-acetylcysteine, p53 inhibitor pifithrin-alpha, and enzyme catalase. Apigenin-mediated p53 activation and apoptosis were further attenuated by p53 antisense oligonucleotide treatment. Exposure of cells to apigenin led to a decrease in the levels of Bcl-XL and Bcl-2 and increase in Bax, triggering caspase activation. Treatment with the caspase inhibitors Z-VAD-FMK and DEVD-CHO partially rescued these cells from apigenin-induced apoptosis. In vivo, apigenin administration demonstrated p53-mediated induction of apoptosis in 22Rv1 tumors. These results indicate that apigenin-induced apoptosis in 22Rv1 cells is initiated by a ROS-dependent disruption of the mitochondrial membrane potential through transcriptional-dependent and -independent p53 pathways.
Indexed as
Identifiers
What OpenQuestion holds
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.