TRIM25 contributes to the malignancy of acute myeloid leukemia and is negatively regulated by microRNA-137.

Background: Acute myeloid leukemia (AML) is a ubiquitous malignancy that occurs in the hematological system. Tripartite motif-containing 25 (TRIM25) has been found to be involved in various carcinomas comprising AML. However, the function and underlying causative role of TRIM25 in AML are still obscure.

Methods: Quantitative real-time polymerase chain reaction (qPCR) was used for assaying TRIM25 and miR-137 expression in AML samples and cells. CCK-8 assay, Calcein-acetoxymethylester/propidium iodide staining, and Transwell assay were adopted to assay cell proliferation, invasion, and migration. Dual-luciferase reporter experiment was used for analyzing the interaction of TRIM25 with miR-137. Western blot was used for assaying protein expression levels.

Results: This study confirmed that TRIM25 expression was upregulated in AML samples and cell lines, whereas miR-137 expression was downregulated. Overexpression of TRIM25 significantly contributed to AML cell's proliferation, invasion, and migration, whereas knockdown exerted the opposite effect. In addition, TRIM25 was a downstream target of miR-137 in AML cells and negatively modulated by miR-137.

Conclusions: TRIM25 was targeted and regulated by miR-137, exerted a carcinogenic function in AML, and could be used as a latent biomarker and a treatment target for AML.