MicroRNA-582–3p negatively regulates cell proliferation and cell cycle progression in acute myeloid leukemia by targeting cyclin B2

Cellular & Molecular Biology Letters

Xuefei Tian¹  Ronghua Xu²  Tian Nie²  Haixia Li³  Paoqiu Wang³  Mao Huang⁴ 

[1] College of Integrated Chinese and Western Medicine, Hunan University of Chinese Medicine;Department of Hematology, The First Hospital of Hunan University of Chinese Medicine;Department of Integrated Chinese and Western Medicine, Hunan Children’s Hospital;Department of Pediatric Rehabilitation, Hebei Provincial Hospital of Traditional Chinese Medicine;

关键词: Acute myeloid leukemia;    miR-582–3p;    Cell cycle;    CCNB2;   

DOI  :  10.1186/s11658-019-0184-7

来源: DOAJ

【 摘 要 】

Abstract Background MicroRNAs (miRNAs) function as post-transcriptional gene expression regulators. Some miRNAs, including the recently discovered miR-582–3p, have been implicated in leukemogenesis. This study aimed to reveal the biological function of miR-582–3p in acute myeloid leukemia (AML), which is one of the most frequently diagnosed hematological malignancies. Methods The expression of miR-582–3p was determined using quantitative real-time PCR in blood samples from leukemia patients and in cell lines. Cell proliferation and cell cycle distribution were analyzed using the CCK-8, colony formation and flow cytometry assays. The target gene of miR-582–3p was verified using a dual-luciferase reporter assay. The G2/M phase arrest-related molecule contents were measured using western blotting analysis. Results We found miR-582–3p was significantly downregulated in the blood samples from leukemia patients and in the cell lines. MiR-582–3p overexpression significantly impaired cell proliferation and induced G2/M cell cycle arrest in THP-1 cells. Furthermore, cyclin B2 (CCNB2) was confirmed as a target gene of miR-582–3p and found to be negatively regulated by miR-582–3p overexpression. More importantly, CCNB2 knockdown showed suppressive effects on cell proliferation and cell cycle progression similar to those caused by miR-582–3p overexpression. The inhibitory effects of miR-582–3p overexpression on cell proliferation and cell cycle progression were abrogated by CCNB2 transfection. Conclusion These findings indicate new functions and mechanisms for miR-582–3p in AML development. Further study could clarify if miR-582–3p and CCNB2 are potential therapeutic targets for the treatment of AML.

【 授权许可】

Unknown