Format

Send to

Choose Destination
Int J Stem Cells. 2018 Nov 30;11(2):227-234. doi: 10.15283/ijsc18053.

The Pharmacological Inhibition of ERK5 Enhances Apoptosis in Acute Myeloid Leukemia Cells.

Author information

1
Department of Stem Cell Biology, School of Medicine, Konkuk University, Seoul, Korea.
2
Stem Cell Research Center, Jeju National University, Jeju, Korea.
3
Mirae Cell Bio Co. LTD, Seoul, Korea.

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.

KEYWORDS:

Acute myeloid leukemia; Apoptosis; Cell cycle; ERK5; XMD8-92

PMID:
30343550
DOI:
10.15283/ijsc18053
Free full text

Supplemental Content

Full text links

Icon for Inforang
Loading ...
Support Center