Abstract
BACKGROUND: Acute myeloid leukemia (AML) is the most common form of acute leukemia in adults. Long non-coding RNA taurine-upregulated gene 1 (lncRNA TUG1) has been discovered to participate in multiple cancers including AML. However, the detailed mechanism of TUG1 in AML remains obscure. MATERIALS AND METHODS: AML cell lines HL-60 and Kasumi-1 were taken as cell models. TUG1 knockdown or overexpression cell lines were generated. Then, the biological influence of TUG1 on cancer cells was studied using CCK-8 assay, transwell assay and Western blot in vitro. Interaction between TUG1 and miR-370-3p was determined by bioinformatics analysis, RT-PCR, and luciferase assay. Western blot, RT-PCR, and luciferase assay were carried out to validate the interaction between miR-370-3p and its target gene Mitogen-Activated Protein Kinase 1 (MAPK1). RESULTS: Knockdown of TUG1 markedly reduced viability and metastasis of AML cells, while its overexpression had the opposite effect. MAPK1 was verified as a target gene of miR-370-3p. TUG1 could reduce the level of functional miR-370-3p, facilitate MAPK1 expression, and in turn activate ERK1/2 signaling. CONCLUSION: TUG1 could modulate malignant phenotypes of AML cells via miR-370-3p/MAPK1/ERK signaling. Our study would help to clarify the mechanism of AML tumorigenesis and progression.