Armillaridin induces autophagy-associated cell death in human chronic myelogenous leukemia K562 cells
| Autor: | Huey-Lan Huang, Chien-Chih Chen, Wei-Pang Huang, Wen-Han Chang, Yu-Jen Chen |
|---|---|
| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
Programmed cell death Blotting Western Apoptosis Biology 03 medical and health sciences Leukemia Myelogenous Chronic BCR-ABL Positive Proto-Oncogene Proteins hemic and lymphatic diseases Autophagy Tumor Cells Cultured medicine Humans Cell Proliferation U937 cell Cell Cycle Membrane Proteins General Medicine Flow Cytometry medicine.disease Mitochondria Acute Monoblastic Leukemia Leukemia 030104 developmental biology Drug Resistance Neoplasm Caspases Cancer research Sesquiterpenes K562 cells Chronic myelogenous leukemia |
| Zdroj: | Tumor Biology. 37:14291-14300 |
| ISSN: | 1423-0380 1010-4283 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full text from SpringerLink