ArticleOpen medicine (Warsaw, Poland)2021
TRIM25 contributes to the malignancy of acute myeloid leukemia and is negatively regulated by microRNA-137.
Article in Open medicine (Warsaw, Poland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- The impact of scaRNA12 deregulation on p53-mediated cellular stress response in B-cell precursor acute lymphoblastic leukaemia.British journal of haematology · 2026Article
- NUP214 in Acute Myeloid Leukemia.Cells · 2025Review
- Review
- Role of MicroRNAs in Acute Myeloid Leukemia.Genes · 2025Review
- Article
- The impact of COVID-19 on microRNA and CD marker expression in AML patients.Scientific reports · 2024Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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 MATERIALS: 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.
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.
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