The Pharmacological Inhibition of ERK5 Enhances Apoptosis in Acute Myeloid Leukemia Cells
International Journal of Stem Cells
; : 227-234, 2018.
Article
in En
| WPRIM
| ID: wpr-739924
Responsible library:
WPRO
ABSTRACT
Acute myeloid leukemia (AML) is a fatal hematological malignancy which is resistant to a variety of chemotherapy drugs. Extracellular signal-regulated kinase 5 (ERK5) plays a novel role in chemoresistance in some cancer cells and this pathway is a central mediator of cell survival and apoptotic regulation. The aim of this study was to investigate the effect of ERK5 inhibitor, XMD8-92, on proliferation and apoptosis in AML cell lines. Findings showed that XMD8-92 inhibited the activation of ERK5 by G-CSF and decreased the expression of c-Myc and Cyclin D1. The treatment of XMD8-92 reduced the phosphorylation of ERK5 leading to a distinct inhibition of cell proliferation and increased apoptosis in Kasumi-1 and HL-60 cells. Taken together, our study suggests that the inhibition of ERK5 by XMD8-92 can trigger apoptosis and inhibit proliferation in AMLs. Therefore, the inhibition of ERK5 may be an effective adjuvant in AML chemotherapy.
Key words
Full text:
1
Database:
WPRIM
Main subject:
Phosphorylation
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Leukemia, Myeloid, Acute
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Cell Cycle
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Cell Line
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Cell Survival
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Granulocyte Colony-Stimulating Factor
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Apoptosis
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HL-60 Cells
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Hematologic Neoplasms
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Cyclin D1
Limits:
Humans
Language:
En
Journal:
International Journal of Stem Cells
Year:
2018
Document type:
Article