Inositol hexaphosphate-induced cellular response in myeloid leukemia cells is mediated by nicotinamide adenine dinucleotide phosphate oxidase activation.
Fujita Med J
; 5(4): 98-103, 2019.
Article
em En
| MEDLINE
| ID: mdl-35111510
ABSTRACT
OBJECTIVES:
The objective of this study was to identify the role of reactive oxygen species (ROS) generated by nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, in inositol hexaphosphate (IP6)-induced metabolic disruption in human leukemia PLB-985 cells.METHODS:
PLB-985 and X chromosome linked gp91-phox gene knockout (X-CGD) cells were treated with 5, 10, or 20 mM IP6 for 24 to 72 h. Cell growth was assayed using a highly water-soluble tetrazolium salt. The rate of apoptotic and necrotic cell death was determined with an Annexin V-fluorescein isothiocyanate/propidium iodide kit. The expression of CD11b as a marker of monocytic property and of LC3 as an autophagy marker was tested, using flow cytometry combined with fluorescent antibodies.RESULTS:
Treatment with 5 and 10 mM IP6 for 24 h was found to suppress the growth of both cell lines, though the effect was more dramatic in PLB-985 cells. After 6-h treatment with 20 mM IP6, the necrosis rate of PLB-985 cells was significantly greater than that of X-CGD cells. Further, after 72-h treatment with 10 mM IP6, CD11b expression was observed in PLB-985 cells but inhibited in X-CGD cells. Autophagy monitoring after 6-h treatment with 10 mM IP6 revealed that LC3 expression was suppressed in PLB-985 cells, whereas it was somewhat increased in X-CGD cells.CONCLUSIONS:
Our results suggest that NADPH oxidase activation mediates IP6-induced metabolic disruption associated with necrosis, differentiation, cell growth, and autophagy in PLB-985 cells.
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Bases de dados:
MEDLINE
Idioma:
En
Revista:
Fujita Med J
Ano de publicação:
2019
Tipo de documento:
Article
País de afiliação:
Japão