MicroRNA-126 attenuates cell apoptosis by targeting TRAF7 in acute myeloid leukemia cells
Acute myeloid leukemia (AML) has a 5-year survival rate of only about 30%–40% due to the self-renewal and differentiation ability of leukemia stem-like cells (LSCs). To address the potential for novel therapeutic targets in LSCs, we investigated the roles of miRNA-126 and tumor necrosis factor recep...
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Published in | Biochemistry and cell biology Vol. 96; no. 6; pp. 840 - 846 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
Canada
NRC Research Press
01.12.2018
Canadian Science Publishing NRC Research Press |
Subjects | |
Online Access | Get full text |
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Summary: | Acute myeloid leukemia (AML) has a 5-year survival rate of only about 30%–40% due to the self-renewal and differentiation ability of leukemia stem-like cells (LSCs). To address the potential for novel therapeutic targets in LSCs, we investigated the roles of miRNA-126 and tumor necrosis factor receptor-associated factor 7 (TRAF7) in AML. We used qRT-PCR and Western blot to investigate the expression levels of miRNA-126 and TRAF7 in AML cell lines. Then, we uncovered the effect of miRNA-126 on AML cell proliferation and apoptosis by MTT assay and flow cytometric analysis, respectively. Furthermore, dual-luciferase assay and Western blot were used to determine the target of miRNA-126 in AML and the potential mechanism by which cell apoptosis is suppressed by miRNA-126. We found that miRNA-126 was highly expressed in all of the AML cell lines, and that inhibition of miRNA-126 significantly induced cell death through apoptosis. The suppression of apoptosis in AML with high expression of miRNA-126 was caused by down-regulating TRAF7, which blocked the c-FLIP pathway. The role of miRNA-126 in AML makes it a potential therapeutic target to improve clinical outcomes for patients with AML. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0829-8211 1208-6002 |
DOI: | 10.1139/bcb-2018-0017 |