Eur Rev Med Pharmacol Sci 2019; 23 (3 Suppl): 224-231
DOI: 10.26355/eurrev_201908_18651

LncRNA-H19 inhibits apoptosis of acute myeloid leukemia cells via targeting miR-29a-3p

T.-T. Zhao, X. Liu

Department of Laboratory Medicine, Affiliated Municipal Hospital of Xuzhou Medical University, Xuzhou, China. liuxin19730512@163.com


OBJECTIVE: To explore the influences of long non-coding ribonucleic acid (lncRNA)-H19 on the proliferation and apoptosis of acute myeloid leukemia (AML) cells via the Wnt signaling pathway.

PATIENTS AND METHODS: Blood samples were collected from 40 AML patients. The AML cells were cultured. Cell counting kit-8 (CCK-8) was used to detect cell proliferation and flow cytometry was applied to analyze cell cycle and determine the apoptosis rate. Moreover, the action target of lncRNA-H19 was detected through a dual-luciferase reporter assay and Western blotting was performed to detect the change in protein level.

RESULTS: The expression of lncRNA-H19 in AML patients was markedly higher than that in normal controls and compared with human embryonic kidney (HEK)-293T cells, AML cell Kasumi-1 exhibited an increased lncRNA-H19 expression. LncRNA-H19 could promote cell proliferation, but suppress cell apoptosis. It is bound to micro RNA (miR)-29a-3p in a targeted manner. and the expression level of miR-29a-3p in AML patients was prominently lower than that in normal controls. After miR-29a-3p was inhibited, the expression of intranuclear β-catenin was significantly increased and the Wnt/β-catenin pathway critical molecules T-cell factor (TCF) and lymphoid enhancer factor 1 (LEF1) were evidently up-regulated after the down-regulation of miR-29a-3p.

CONCLUSIONS: LncRNA-H19 targets miR-29a-3p to promote the proliferation of AML cells, but inhibit the apoptosis through the Wnt/ β-catenin signaling pathway.

Published on: 2019/08/07


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To cite this article

T.-T. Zhao, X. Liu
LncRNA-H19 inhibits apoptosis of acute myeloid leukemia cells via targeting miR-29a-3p

Eur Rev Med Pharmacol Sci
Year: 2019
Vol. 23 - N. 3 Suppl
Pages: 224-231
DOI: 10.26355/eurrev_201908_18651