Sheng Wang1, Bang Shuo Zhang1, Yi Yang1, Ying Li1, Jing Long Lv1, Yu Cheng2. 1. Department of Hematology, Three Gorges Hospital Affiliated to Chongqing University, Chongqing, 404000, China. 2. Department of Gastroenterology, Three Gorges Hospital Affiliated to Chongqing University, No. 165 Xincheng Road, Wanzhou District, Chongqing, 404000, China.
Abstract
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 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. 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. CONCLUSION: 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.
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 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. 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. CONCLUSION: 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.
Authors: Kim R Kampen; Frank J G Scherpen; Hasan Mahmud; Arja Ter Elst; André B Mulder; Victor Guryev; Han J M P Verhagen; Kim De Keersmaecker; Linda Smit; Steven M Kornblau; Eveline S J M De Bont Journal: Cancer Res Date: 2018-09-05 Impact factor: 12.701