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Updated: May 15, 2025

Proliferation and Differentiation of Murine Myeloid Precursor 32D/G-CSF-R Cells
Published on: February 21, 2018
Circ_0035381 contributes to the progression of acute myeloid leukemia via regulating miR-186-5p/CDCA3 pathway
Jinhuan Xu1, Xi Ming1, Jiaying Wu1
1Department of Hematology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan City, Hubei Province, China.
Background:
Circular RNAs (circRNAs) are involved in acute myeloid leukemia (AML) and may be useful for AML therapy. Herein, the project aimed to explore the functions and mechanisms of circ_0035381 in AML.
Research Design And Methods:
Circ_0035381, microRNA-186-5p (miR-186-5p), and cell division cycle associated 3 (CDCA3) expression were determined using quantitative real-time polymerase chain reaction (qRT-PCR) assay. Western blot assay was used to measure protein levels. 5'-ethynyl-2'-deoxyuridine (EdU) and flow cytometry were adopted to measure cell proliferation and apoptosis. Glucose consumption and lactate uptake were examined with commercial kits. The relationships between miR-186-5p and circ_0035381 or CDCA3 were validated using dual-luciferase reporter and RNA pull-down assays.
Results:
Circ_0035381 was increased in the AML subject and AML cell line. Circ_0035381 deficiency hindered the proliferation and glycolysis level and promoted apoptosis in the AML cell line. Circ_0035381 sponged miR-186-5p and miR-186-5p inhibition reversed the effect of circ_0035381 knockdown on AML cell progression. CDCA3 was the target gene of miR-186-5p. CDCA3 overexpression reversed circ_0035381 knockdown-mediated AML cell proliferation and glycolysis inhibition and apoptosis promotion.
Conclusions:
Circ_0035381 promoted AML progression by elevating CDCA3 through sponging miR-186-5p, providing some clues for the diagnosis and treatment of AML.
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