ArticleCell death & disease2014
Medicarpin, a legume phytoalexin sensitizes myeloid leukemia cells to TRAIL-induced apoptosis through the induction of DR5 and activation of the ROS-JNK-CHOP pathway.
Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 77 citations in OpenAlex.
- Enhanced Inhibition ofInternational journal of molecular sciences · 2026Article
- Network Pharmacology and Molecular Docking Identify Medicarpin as a Potent CASP3 and ESR1 Binder Driving Apoptotic and Hormone-Dependent Anticancer Activity.International journal of molecular sciences · 2025Article
- Computational Investigation Identifies mTOR as a Primary Binding Target of Medicarpin in Cholangiocarcinoma: Insights from Network Pharmacology and Molecular Docking.Life (Basel, Switzerland) · 2025Article
- Review
- Biotransformation of medicarpin from homopterocarpin by Aspergillus niger and its biological characterization.Scientific reports · 2025Article
- Role of Phytoconstituents in Cancer Treatment: A Review.Recent advances in food, nutrition & agriculture · 2024Review
- Licochalcone A Exerts Anti-Cancer Activity by Inhibiting STAT3 in SKOV3 Human Ovarian Cancer Cells.Biomedicines · 2023Article
- Natural Products as Anticancer Agents: Current Status and Future Perspectives.Molecules (Basel, Switzerland) · 2022Review
- Cytotoxicity ofMolecules (Basel, Switzerland) · 2022Article
- Medicarpin Increases Antioxidant Genes by Inducing NRF2 Transcriptional Level in HeLa Cells.Antioxidants (Basel, Switzerland) · 2022Article
- Medicarpin Protects Cerebral Microvascular Endothelial Cells Against Oxygen-Glucose Deprivation/Reoxygenation-Induced Injury via the PI3K/Akt/FoxO Pathway: A Study of Network Pharmacology Analysis and Experimental Validation.Neurochemical research · 2022Article
- In vitro propagation from axillary buds of the endangered treePlant biotechnology (Tokyo, Japan) · 2021Article
- Downregulation of Diacylglycerol kinase zeta (DGKZ) suppresses tumorigenesis and progression of cervical cancer by facilitating cell apoptosis and cell cycle arrest.Bioengineered · 2021Article
- Alternol Sensitizes Renal Carcinoma Cells to TRAIL-Induced Apoptosis.Frontiers in pharmacology · 2021Article
- VDMolecular biology reports · 2020Article
- Non-Thermal Plasma Couples Oxidative Stress to TRAIL Sensitization through DR5 Upregulation.International journal of molecular sciences · 2020Article
- Lessons from Exploring Chemical Space and Chemical Diversity of Propolis Components.International journal of molecular sciences · 2020Review
- The "Janus" Role of C/EBPs Family Members in Cancer Progression.International journal of molecular sciences · 2020Review
- Oxidative resistance of leukemic stem cells and oxidative damage to hematopoietic stem cells under pro-oxidative therapy.Cell death & disease · 2020Review
- Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor necrosis factor α-related apoptosis-inducing ligand (TRAIL) is a promising anticancer agent with cancer cell-selective cell death inducing effect. However, the major limitation in the usage of TRAIL as a chemotherapeutic agent is the development of TRAIL resistance in many cancer types including myeloid leukemia. In this study, we report for the first time that Medicarpin (Med), a naturally occurring phytoalexin sensitizes myeloid leukemia cells to TRAIL-induced apoptosis. Combination of Med and TRAIL induced significantly higher apoptosis compared with that of the individual treatments of either agent alone through activation of both the extrinsic and the intrinsic cell death pathways characterized by the activation of caspases 8, 9, 3, and 7. Med treatment downregulated antiapoptotic proteins (Survivin, Bcl2, Bcl-xL, XIAP, and c-FLIP), upregulated pro-apoptotic proteins (Bax, Cytochrome C, Smac/Diablo, Bid, truncated Bid (tBid), p-eIF2α, Bip, and CHOP (CCAAT-enhancer binding protein homologous protein)), induced G2/M cell-cycle arrest, and increased the expression of the functional TRAIL receptor DR5 through activation of the ROS-JNK-CHOP pathway. Gain and loss of function studies clearly indicated that DR5 expression was critical for Med-induced TRAIL sensitization. The Med-induced TRAIL sensitization did not involve the NFkB signaling pathway or redistribution of DR5 in lipid rafts. The concomitant treatment with Med and TRAIL showed robust apoptotic effects in primary myeloid leukemia cells but had no toxic effects in primary human peripheral blood mononuclear cells (PBMCs). In conclusion, our results suggest that Med sensitizes myeloid leukemia cells to TRAIL-induced apoptosis through the upregulation of DR5 through activation of the ROS-JNK-CHOP pathway.
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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.