Lin Li-Ping, Zhang Qian, Wu Wei, Xue Yan, Tang Yong-Jin, Lin Dong-Hong
The School of Medical Technology and Engineering, Fujian Medical University, Fuzhou 350004, Fujian Province, China.
The School of Medical Technology and Engineering, Fujian Medical University, Fuzhou 350004, Fujian Province, China,E-mail:
Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2020 Dec;28(6):1853-1858. doi: 10.19746/j.cnki.issn.1009-2137.2020.06.011.
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).
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.
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).
MiR-29b-3p can inhibit the proliferation and induce apoptosis of AML cells by down-regulating STAT3.
通过靶向信号转导和转录激活因子3（STAT3）来研究miR-29b-3p对急性髓系白血病（AML）细胞凋亡和增殖的影响。
使用TargetScan和miRanda在线数据库预测miR-29b-3p与STAT3 3'UTR的结合位点。通过双荧光素酶报告基因检测实验评估它们之间的靶向关系。在miR-29b-3p过表达后，使用qPCR和蛋白质印迹法检测STAT3 mRNA和蛋白质的表达，通过流式细胞术测定AML细胞的凋亡情况，并使用MTS检测每组细胞增殖的变化。
双荧光素酶报告基因检测证实STAT3是miR-29b-3p的靶基因。miR-29b-3p过表达后，STAT3 mRNA和蛋白质的表达降低。与对照组相比，过表达组中AML细胞的增殖减少，凋亡增加（P<0.05）。
MiR-29b-3p可通过下调STAT3来抑制AML细胞的增殖并诱导其凋亡。
