Li-Ping Lin1, Qian Zhang1, Wei Wu1, Yan Xue1, Yong-Jin Tang1, Dong-Hong Lin2. 1. The School of Medical Technology and Engineering, Fujian Medical University, Fuzhou 350004, Fujian Province, China. 2. The School of Medical Technology and Engineering, Fujian Medical University, Fuzhou 350004, Fujian Province, China,E-mail: lindh65@163.com.
Abstract
OBJECTIVE: To investigate the effect of miR-29b-3p on apoptosis and proliferation of acute myeloid leukemia (AML) cells by targeting signal transducer and activator of transcription 3 (STAT3). METHODS: TargetScan and miRanda online databases were used to predict the binding sites of miR-29b-3p and STAT3 3'UTR. The targeting relationship between them was estimated by Dual-Luciferase reporter assay experiment. After miR-29b-3p over-expression, qPCR and Western blot were used to detect the expression of STAT3 mRNA and proteins, flow cytometry to determine the apoptosis of AML cells, and MTS to detect the changes of cell proliferation in each group. RESULTS: Dual-Luciferase reporter assay confirmed that STAT3 was the target gene of miR-29b-3p. After miR-29b-3p overexpression, the expression of STAT3 mRNA and protein decreased. Compared with the control groups, the proliferation of AML cells in the overexpression group decreased and the apoptosis increased (P<0.05). CONCLUSION: MiR-29b-3p can inhibit the proliferation and induce apoptosis of AML cells by down-regulating STAT3.
OBJECTIVE: To investigate the effect of miR-29b-3p on apoptosis and proliferation of acute myeloid leukemia (AML) cells by targeting signal transducer and activator of transcription 3 (STAT3). METHODS: TargetScan and miRanda online databases were used to predict the binding sites of miR-29b-3p and STAT3 3'UTR. The targeting relationship between them was estimated by Dual-Luciferase reporter assay experiment. After miR-29b-3p over-expression, qPCR and Western blot were used to detect the expression of STAT3 mRNA and proteins, flow cytometry to determine the apoptosis of AML cells, and MTS to detect the changes of cell proliferation in each group. RESULTS: Dual-Luciferase reporter assay confirmed that STAT3 was the target gene of miR-29b-3p. After miR-29b-3p overexpression, the expression of STAT3 mRNA and protein decreased. Compared with the control groups, the proliferation of AML cells in the overexpression group decreased and the apoptosis increased (P<0.05). CONCLUSION: MiR-29b-3p can inhibit the proliferation and induce apoptosis of AML cells by down-regulating STAT3.