ArticleCancer medicine2019
Cordycepin-induced unfolded protein response-dependent cell death, and AKT/MAPK-mediated drug resistance in mouse testicular tumor cells.
Article in Cancer medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.
- A Systematic Review of the Biological Effects of Cordycepin.Molecules (Basel, Switzerland) · 2021Pooled it
- The Inclusion of Dietary and Medicinal Mushrooms into Translational Oncology: Pros and Cons at the Molecular Level.International journal of molecular sciences · 2026Review
- Mechanisms of cisplatin sensitivity and resistance in testicular germ cell tumors and potential therapeutic agents (Review).Experimental and therapeutic medicine · 2025Review
- Cordycepin generally inhibits growth factor signal transduction in a systems pharmacology study.FEBS letters · 2025Article
- Integrating network pharmacology, quantitative transcriptomic analysis, and experimental validation revealed the mechanism of cordycepin in the treatment of obesity.Frontiers in pharmacology · 2025Article
- Application and research progress of cordycepin in the treatment of tumours (Review).Molecular medicine reports · 2024Review
- Metabolites and Their Bioactivities from the GenusMicroorganisms · 2022Review
- Cordycepin enhances radiosensitivity to induce apoptosis through cell cycle arrest, caspase pathway and ER stress in MA-10 mouse Leydig tumor cells.American journal of cancer research · 2022Article
- The Role of Autophagy in Anti-Cancer and Health Promoting Effects of Cordycepin.Molecules (Basel, Switzerland) · 2021Review
- Anti-Cancer Effect of Cordycepin on FGF9-Induced Testicular Tumorigenesis.International journal of molecular sciences · 2020Article
- Cordycepin-induced unfolded protein response-dependent cell death, and AKT/MAPK-mediated drug resistance in mouse testicular tumor cells.Cancer medicine · 2019Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Testicular cancer is the most commonly diagnosed cancer in men at 15-44 years of age, and radical orchidectomy combined with chemotherapy is currently considered as the standard treatment. However, drugs resistance and side effects that impact the quality of life for patients with testicular cancer have not been markedly improved in recent decades. In this study, we characterized the pharmacological exacerbation of the unfolded protein response (UPR), which is an effective approach to kill testicular cancer cells, by carrying out a clustering analysis of mRNA expression profiles and the immunobloting examination of cordycepin-treated MA-10 cells. The UPR is executed in response to endoplasmic reticulum stress to complement by an apoptotic response if the defect cannot be resolved. Results showed that cordycepin significantly modulated FoxO/P15/P27, PERK-eIF2α (apoptotic), and the IRE1-XBP1 (adaptive) UPR pathways. Interestingly, a fraction of MA-10 cells survived after cordycepin treatment, the AKT, LC3 I/II, and MAPK signaling pathways were highly induced in attached cells as compared to the suspended cells, illustrating the drug resistance to cordycepin via activating AKT and MAPK pathways in MA-10 cells. In summary, PERK-eIF2α signaling pathway is required for pro-apoptotic UPR in MA-10 cell death following cordycepin treatment, suggesting a potential therapeutic application in treating testicular cancer. However, activation of AKT and MAPK pathways could possibly result in drug resistance to cordycepin in MA-10 cells.
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