ArticleDrug design, development and therapy2018
Chrysin suppresses proliferation, migration, and invasion in glioblastoma cell lines via mediating the ERK/Nrf2 signaling pathway.
Article in Drug design, development and therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.
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Who cites it
52 citing papers in PubMed, 1 synthesis or guideline pooled it, 93 citations in OpenAlex.
- Overexpressed XRCC2 as an independent risk factor for poor prognosis in glioma patients.Molecular medicine (Cambridge, Mass.) · 2021Pooled it
- Natural Compounds Targeting Oncogenic Signaling Networks in Glioblastoma: Molecular Mechanisms, Translational Advances, and Clinical Perspectives.Brain and behavior · 2026Review
- Multiscale analysis and optimal glioma therapeutic candidate discovery using the CANDO platform.Journal of cheminformatics · 2026Article
- Illuminating the pleiotropic effects of bixin-loaded nanoemulsion on glioblastoma cell behavior through an integrated approach.Molecular biology reports · 2026Article
- Chitosan-functionalized mesoporous silica nanoparticles co-loaded with chrysin and quercetin: a potent strategy against lung cancer cells.Scientific reports · 2026Article
- Identifying Key Pathogenic Mechanisms in Recurrent Glioblastoma Through Bioinformatics Analysis.Current medicinal chemistry · 2026Article
- Dual-metallic porphyrinic MOFs with pH/ROS-responsive release for antibacterial and antioxidant therapy of diabetic infected wounds.Theranostics · 2026Article
- Chrysin as a Multifunctional Therapeutic Flavonoid: Emerging Insights in Pathogenesis Management: A Narrative Review.International journal of molecular sciences · 2025Review
- Oxidative Stress and Antioxidants in Glioblastoma: Mechanisms of Action, Therapeutic Effects and Future Directions.Antioxidants (Basel, Switzerland) · 2025Review
- Protective Effects of Chrysin Against Diclofenac-Induced Nephrotoxicity in Rats via Attenuation of Oxidative Stress, Apoptosis and Endoplasmic Reticulum Stress.Journal of biochemical and molecular toxicology · 2025Article
- Chrysin sensitizes glioblastoma cells and spheroids to temozolomide treatment by reducing EMT and stemness phenotypes, as well as targeting multidrug resistance proteins.Frontiers in pharmacology · 2025Article
- Roles of Phytochemicals in Cancer Prevention and Therapeutics.International journal of molecular sciences · 2024Article
- Nrf2 Pathway and Oxidative Stress as a Common Target for Treatment of Diabetes and Its Comorbidities.International journal of molecular sciences · 2024Review
- Keap1-Nrf2 pathway: a key mechanism in the occurrence and development of cancer.Frontiers in oncology · 2024Review
- Co-administration of Chrysin and Luteolin with Cisplatin and Topotecan Exhibits a Variable Therapeutic Value in Human Cancer Cells, HeLa.ACS omega · 2023Article
- Unraveling the signaling mechanism behind astrocytoma and possible therapeutics strategies: A comprehensive review.Cancer reports (Hoboken, N.J.) · 2023Review
- Alkaloids as Natural NRF2 Inhibitors: Chemoprevention and Cytotoxic Action in Cancer.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Temozolomide Resistance in Glioblastoma by NRF2: Protecting the Evil.Biomedicines · 2023Review
- Review
- Niosomes nanoparticles as a novel approach in drug delivery enhances anticancer properties of chrysin in human ovarian carcinoma cells (SKOV3): an in vitro study.Medical oncology (Northwood, London, England) · 2023Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundChrysin, an active natural bioflavonoid, has been proven to protect against carcinogenesis. However, the role of chrysin in glioblastoma and the potential molecular mechanisms remain to be elucidated. In our previous study, we found that nuclear factor erythroid 2 (NF-E2)-related factor 2 (Nrf2) is highly expressed in a variety of glioblastoma cell lines associated with the mitogen-activated protein kinase (MAPK) pathway. The aim of this study was to evaluate the antitumor effects of chrysin in glioblastoma cells and how chrysin is related to the MAPK/Nrf2 signaling pathway.
methodsA Cell Counting Kit-8 assay and a plate colony formation assay were performed to evaluate cell proliferation. Cell migration ability was tested by a wound-healing assay. Transwell migration and Matrigel invasion assay were used to test the migration and invasion potential of cells. Nrf2 was knocked down by shRNA transfection. Protein expression was determined by Western blotting and immunofluorescence staining. The in vivo anticancer effect was measured using tumor xenografts in nude mice.
resultsChrysin inhibited the proliferation, migration, and invasion capacity of glioblastoma cells in dose- and time-dependent manners. Mechanistically, chrysin deactivated the Nrf2 signaling pathway by decreasing the translocation of Nrf2 into the nucleus and suppressing the expression of hemeoxygenase-1 (HO-1) and NAD(P)H quinine oxidoreductase-1, meanwhile, Nrf2 shRNA attenuated the anticancer activity of chrysin. Furthermore, chrysin downregulated the protein expression of p-extracellular signal-regulated kinase 1 and 2 (ERK1/2), but did not significantly affect p-JNK and p-P38 expression levels. However, the downregulated level of Nrf2 and the antitumor effect of chrysin in glioblastoma cell lines were partially abrogated by the ERK1/2 signaling inhibitor (U0126). Finally, chrysin inhibited tumor growth in U87 xenografts.
conclusionOur results show that chrysin exerts anticancer activity in glioblastoma cell lines possibly via the ERK/Nrf2 signaling pathway and indicate the potential application of chrysin as a natural sensitizer in chemotherapy.
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