OncoTargets and Therapy (Nov 2019)
Long Non-Coding RNA TUG1 Modulates Proliferation, Migration, And Invasion Of Acute Myeloid Leukemia Cells Via Regulating miR-370-3p/MAPK1/ERK
Abstract
Gang Li, Peiming Zheng, Huiling Wang, Yushu Ai, Xiaohuan Mao Department of Clinical Laboratory, Henan Provincial People’s Hospital, People’s Hospital of Zhengzhou University, Zhengzhou 450003, Henan, People’s Republic of ChinaCorrespondence: Xiaohuan MaoDepartment of Clinical Laboratory, Henan Provincial People’s Hospital, People’s Hospital of Zhengzhou University, Weiwu Road, No. 7, Zhengzhou 450003, Henan, People’s Republic of ChinaEmail [email protected]: 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.Keywords: LncRNA, TUG1, AML, miR-370-3p, MAPK1
