Abstract
Background: Acute myeloid leukemia (AML) is a serious threat to human health. Long non-coding RNA (lncRNA) Taurine-Upregulated Gene1 (TUG1) has been reported to participate in the development and progression of several cancers, including AML. Herein, we aimed to investigate the pathognomonic role of TUG1 in AML cells and its potential mechanistic pathway. Methods: Quantitative real-time PCR (qRT-PCR) assay was applied to detect the expression levels of lncRNA TUG1, miR-193a-5p and Rab10 in AML bone marrow and cell lines. The CCK-8 assay was conducted to assess the cell viability of AML HL-60 and NB4 cells and cell apoptotic assay was performed to assess the cell death. Dual-luciferase reporter assay was carried out to clarify the relationships among TUG1, miR-193a-5p and Rab10. Also, the protein level of Rab10 was examined by Western blot assay. Results: LncRNA TUG1 was up-regulated in AML bone marrow and cells. Functional analysis showed that the silencing of TUG1 suppressed cell viability, while promoted cell death in AML HL-60 and NB4 cells. TUG1 targeted miR-193a-5p and negatively regulated miR-193a-5p expression. Overexpressed miR-193a-5p resulted in the decrease of cell viability and the increase in the cell death in AML cells. Restoration experiments proved that TUG1 regulated the cell viability and death of AML cells through regulating the miR-193a-5p/Rab10 axis. Rab10 was a direct target of miR-193a-5p and was inversely regulated by miR-193a-5p. TUG1 regulated the cell viability and death of AML cells through upregulating Rab10. Conclusion: Silencing of lncRNA TUG1 induces a cytotoxic effect on AML cell lines through sponging miR-193a-5p and the suppression of Rab10.