Abstract
BackgroundAcute 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 and materialsQuantitative 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.ResultsThis 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.ConclusionTRIM25 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.
Highlights
Acute myeloid leukemia (AML) is the most common hematological malignancy in the world blood system characterized by the proliferation and infiltration of clonal, abnormally differentiated hemopoietic stem cells in bone marrow, as well as peripheral blood, etc. [1]
This study explored the interaction between Tripartite motif-containing 25 (TRIM25) and miR-137 to reveal their potential mechanisms in the malignant progression of AML
QPCR was applied for assaying the TRIM25 mRNA level in the blood samples of 45 patients with AML and 45 healthy volunteers
Summary
Acute myeloid leukemia (AML) is the most common hematological malignancy in the world blood system characterized by the proliferation and infiltration of clonal, abnormally differentiated hemopoietic stem cells in bone marrow, as well as peripheral blood, etc. [1]. Researches evidenced that the TRIM family has antiviral effects and actively participates in modulating cell differentiation, proliferation, apoptosis, and tumorigenesis [7]. MicroRNA (miRNA) is a type of small RNA without coding function but has a length of 21–25 nucleotides It is a significant factor in gene modulation by suppressing. The abnormal expression of miRNA is closely connected to cancer progression, making it a latent marker for carcinoma prognosis and diagnosis [14]. MiR-137 belongs to the miRNA family and has been revealed to suppress cancer in various cancers’ progress. This study explored the interaction between TRIM25 and miR-137 to reveal their potential mechanisms in the malignant progression of AML. TRIM25 expression is negatively modulated by miR-137, which participates in facilitating AML cell’s proliferation, invasion, and migration
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