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Updated: Feb 18, 2026

Proliferation and Differentiation of Murine Myeloid Precursor 32D/G-CSF-R Cells
Published on: February 21, 2018
MiR-182-5p regulates BCL2L12 and BCL2 expression in acute myeloid leukemia as a potential therapeutic target
Suwei Zhang1, Qiaoxin Zhang2, Ganggang Shi3
1Department of Pharmacology, Shantou University Medical College, Shantou, Guangdong, China; Department of Clinical Laboratory Medicine, Shantou Central Hospital, Guangdong, China.
Abstract:
The importance of microRNAs (miRNAs) are shown during various cancers including acute myeloid leukemia (AML). MiR-182-5p functions as an oncogene or a potential suppressive miRNA in cancers, but its expression and function in AML is unknown. The purpose is to investigate the roles of miR-182-5p in AML in this study. MiR-182-5p was examined in the blood samples of AML and it was found that miR-182-5p expression levels were higher in AML tissues than it in their normal controls, so did in the AML cells. BCL2L12 and BCL2 were predicted as target genes of miR-182-5p and verified using luciferase reporter assay. BCL2L12 and BCL2 mRNA and protein levels were up-regulated in the AML cells with miR-182-5p inhibition. Cellular function of miR-182-5p indicated that miR-182-5p suppression in AML cells could decrease cell proliferation and reverse cisplatin (DDP) resistance via targeting BCL2L12 and BCL2 expression. Inhibition of miR-182-5p promoted AML cell apoptosis by targeting BCL2 or BCL2L12. The study demonstrates that high levels of miR-182-5p in AML promotes cell proliferation and suppresses cell apoptosis by targeting BCL2L12 and BCL2.
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