ArticleBiomolecules2025
Methyl Protodioscin Promotes Ferroptosis of Prostate Cancer Cells by Facilitating Dissociation of RB1CC1 from the Detergent-Resistant Membranes and Its Nuclear Translocation.
Article in Biomolecules, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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1 citing paper in PubMed.
- Hexosamine Biosynthetic Pathway and Fatty Acid β-Oxidative Imbalance: A Key Mechanism by Which Abnormal Macrophage Lipophagy Promotes Atherosclerosis in Diabetes.Cardiovascular drugs and therapy · 2026Review
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8 authors.
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Abstract
Methyl protodioscin (MPD), a furostanol saponin found in the rhizomes of Dioscorea plants, has been shown to effectively inhibit proliferation of prostate cancer cells in vitro and in vivo. However, the mechanism underlying this inhibitory action remains unclear. To elucidate the mechanism, we used mass spectrometry to analyze protein rearrangements in detergent-resistant membranes (DRMs). Ferroptosis-related factors were identified in cells in vitro and in vivo. MPD induced the expression of acyl-CoA synthetase long chain family member 4 and reduced expression levels of glutathione peroxidase 4 and solute carrier family 7 member 11. Following MPD treatment, RB1-inducible coiled-coil 1 (RB1CC1) dissociated from DRMs and translocated from the cytoplasm to the nucleus. This translocation induced the expression of ferroptosis-related protein coiled-coil-helix-coiled-coil-helix domain containing 3, promoting ferroptosis in prostate cancer cells. As the nuclear translocation of RB1CC1 was promoted by the JNK signaling pathway, SP600125, a JNK inhibitor, prevented the MPD-induced RB1CC1 nuclear translocation. In summary, MPD induced the dissociation of RB1CC1 from DRMs and its subsequent nuclear translocation, contributing to ferroptosis of prostate cancer cells.
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