ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2016
Armillaridin induces autophagy-associated cell death in human chronic myelogenous leukemia K562 cells.
Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2016. 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, 7 citations in OpenAlex.
- Anticancer Secondary Metabolites Produced by Fungi: Potential and Representative Compounds.International journal of molecular sciences · 2025Review
- Potential Medicinal Fungi from Freshwater Environments as Resources of Bioactive Compounds.Journal of fungi (Basel, Switzerland) · 2025Review
- The Anticancer Potential of Edible Mushrooms: A Review of Selected Species from Roztocze, Poland.Nutrients · 2024Review
- Network Pharmacology Analysis of Liquid-CulturedMolecules (Basel, Switzerland) · 2024Article
- Research Status and Application Prospects of the Medicinal Mushroom Armillaria mellea.Applied biochemistry and biotechnology · 2023Review
- Novel mechanism of napabucasin, a naturally derived furanonaphthoquinone: apoptosis and autophagy induction in lung cancer cells through direct targeting on Akt/mTOR proteins.BMC complementary medicine and therapies · 2022Article
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Authors and funding
5 authors at 5 institutions in 1 country.
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Abstract
Armillaridin (AM) is an aromatic ester compound isolated from Armillaria mellea. Treatment with AM markedly reduced the viability of human chronic myelogenous leukemia K562, chronic erythroleukemia HEL 92.1.7, and acute monoblastic leukemia U937 cells, but not normal human monocytes, in a dose- and time-dependent manner. Treatment of K562 cells with AM caused changes characteristic of autophagy. Only a small amount of AM-treated K562 cells exhibited apoptosis. By contrast, AM treatment resulted in extensive apoptotic features in U937 and HEL 92.1.7 cells without evident autophagy. The autophagy of K562 cells induced by AM involved autophagic flux, including autophagosome induction, the processing of autophagosome-lysosome fusion and downregulation of BCL2/adenovirus E1B 19 kDa interacting protein 3 (BNIP3). By bcr-abl knockdown, the growth inhibition of K562 cells caused by AM was partially blocked, suggesting that AM-induced cell death might be a bcr-abl-dependent mode of autophagy-associated cell death. In conclusion, AM is capable of inhibiting growth and inducing autophagy-associated cell death in K562 cells, but not in normal monocytes. It may have potential to be developed as a novel therapeutic agent against leukemia.
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Registered trials
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.