T-T Zhao1, X Liu. 1. Department of Laboratory Medicine, Affiliated Municipal Hospital of Xuzhou Medical University, Xuzhou, China. liuxin19730512@163.com.
Abstract
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.
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 AMLpatients. 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 AMLpatients was markedly higher than that in normal controls and compared with humanembryonic 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 AMLpatients 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.