ArticleEuropean journal of nutrition2012
Impact of JNK1, JNK2, and ligase Itch on reactive oxygen species formation and survival of prostate cancer cells treated with diallyl trisulfide.
Article in European journal of nutrition, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 18 citations in OpenAlex.
- Dysregulation of Iron Homeostasis Mediated by FTH Increases Ferroptosis Sensitivity in TP53-Mutant Glioblastoma.Neuroscience bulletin · 2025Article
- In Vitro Toxicity Studies of Bioactive Organosulfur Compounds fromFoods (Basel, Switzerland) · 2022Review
- JNK/Itch Axis Mediates the Lipopolysaccharide-Induced Ubiquitin-Proteasome-Dependent Degradation of Ferritin Light Chain in Murine Macrophage Cells.Inflammation · 2022Article
- Postbiotics, Metabolic Signaling, and Cancer.Molecules (Basel, Switzerland) · 2021Review
- Dietary Bioactive Diallyl Trisulfide in Cancer Prevention and Treatment.International journal of molecular sciences · 2017Review
- Hydrogen Sulfide Signaling Axis as a Target for Prostate Cancer Therapeutics.Prostate cancer · 2016Review
- Critical role for reactive oxygen species in apoptosis induction and cell migration inhibition by diallyl trisulfide, a cancer chemopreventive component of garlic.Breast cancer research and treatment · 2013Article
- Upregulation of Circular RNA Itchy E3 Ubiquitin Protein Ligase Inhibits Cell Proliferation and Promotes Cell Apoptosis Through Targeting MiR-197 in Prostate Cancer.Technology in cancer research & treatmentArticle
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeIn our previous study, we demonstrated that diallyl trisulfide (DATS) induced iron-dependent G2-M arrest of prostate cancer cell cycle. Moreover, ferritin degradation and an increase of labile iron pool has been linked to the activation of the JNK signaling axis. In the present work, we extended this study to determine which of the c-jun kinases is responsible for ferritin degradation and the role of iron in DATS-induced cell death. We hypothesized that JNK1 activates Itch ligase which will lead to ferritin ubiquitination, an increase in iron-dependent ROS formation and cell death.
methodsPC-3 prostate cancer cells were used in this study. Cell viability, concentration of ROS, labile iron pool, and changes in ferritin and P-Itch and DNA damage were determined.
resultsWe observed that DATS induced ferritin degradation through JNK, Itch signaling axis. DATS did not induce neither ROS formation nor increase the LIP in JNK1-DN transfected cells. We also observed that DATS increased JNK-dependent activating phosphorylation of E3ligase Itch. The cells transfected with inactive form of Itch were more resistant against cytotoxicity of DATS and showed lower DATS-induced ferritin degradation. Desferrioxamine a specific iron chelator had no effect neither on cell viability nor DNA damage evaluated by comet assay.
conclusionsThese results suggest that JNK1-dependent increase in LIP is mediated by Itch ubiquitin ligase.
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