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.
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.
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.