ArticleFrontiers in oncology2025
Ginsenoside Rh2 repressed the progression of prostate cancer through the mitochondrial damage induced by mitophagy and ferroptosis.
Article in Frontiers in oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Biomimetic photodynamic nanoparticles exert anti-tumor therapy by inducing ferroptosis in non-small cell lung cancer.Materials today. Bio · 2026Article
- Ginsenoside Rh2 inhibits non-small-cell lung cancer malignant progression through targeting AURKA.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Ginsenosides fromJournal of ginseng research · 2026Review
- Ginsenoside Rg3 inhibits melanoma progression by inducing ferroptosis via the p53/SLC7A11/GPX4 pathway.Journal of advanced research · 2026Article
- Programmed cell death mechanisms of traditional plant medicine in prostate cancer therapy.Frontiers in immunology · 2026Review
- Mitochondrial convergence of ferroptosis and cuproptosis in castration-resistant prostate cancer: From metabolic vulnerabilities to therapeutic targeting.BBA advances · 2026Review
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Authors and funding
6 authors.
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Abstract
Introduction: Prostate cancer (PC), the most common male genitourinary malignancy and second leading cause of global cancer deaths in men, frequently progresses to lethal castration-resistant PC (CRPC). Ginsenoside Rh2 (GRh2), a ginseng-derived bioactive compound, exhibits antitumor potential, but its efficacy and mechanisms in PC remain unclear. Methods: PC3 cells were treated with GRh2 to assess proliferation (IC50 calculation), migration, and invasion. Mitochondrial function (membrane potential, ROS, ATP/ADP), mitophagy markers (PINK1/Parkin, VDAC1/TOM20, autophagosomes), and ferroptosis indicators (lipid ROS, MDA, Fe Results: GRh2 potently inhibited PC3 cell proliferation (IC50 = 19.3 μg/mL), migration, and invasion. It induced mitochondrial dysfunction (depolarized membrane, elevated ROS, disrupted ATP/ADP) and activated mitophagy, evidenced by upregulated PINK1/Parkin, reduced VDAC1/TOM20, and autophagosome accumulation. Concurrently, GRh2 triggered ferroptosis via lipid ROS accumulation, increased MDA/Fe Discussion: This study provides the first evidence that GRh2 exerts synergistic antitumor effects in PC through dual induction of mitophagy-associated mitochondrial damage and ferroptosis. The reversibility of both pathways by specific inhibitors establishes a causal mechanistic framework. GRh2 thus represents a multifaceted therapeutic agent against PC by targeting mitochondrial integrity.
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