MicroRNA-126 attenuates cell apoptosis by targeting TRAF7 in acute myeloid leukemia cells

• Published in: Biochemistry and cell biology Vol. 96; no. 6; pp. 840 - 846
• Main Authors: Ding, Qian, Wang, Qing, Ren, Yi, Zhu, Hong Qian, Huang, ZhuYun
• Format: Journal Article
• Language: English
• Published: Canada NRC Research Press 01.12.2018; Canadian Science Publishing NRC Research Press
• Subjects: Acute myeloid leukemia; acute myeloid leukemia cells; apoptose; Apoptosis; Biotechnology; c-FLIP protein; Cancer cells; Cell death; Cell proliferation; Cell self-renewal; cellules de leucémie myéloïde aigüe; Dosage; FLIP protein; Flow cytometry; Genetic aspects; Health aspects; Leukemia; miARN-126; MicroRNA; miRNA; miRNA-126; Myeloid leukemia; Ribonucleic acid; RNA; Survival; Therapeutic applications; TRAF7; TRAF7; miRNA-126; cellules de leucémie myéloïde aigüe; miARN-126; acute myeloid leukemia cells; apoptosis; apoptose
• ISSN: 0829-8211; 1208-6002
• DOI: 10.1139/bcb-2018-0017

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.