[MiR-181a Promotes Proliferation of Human Acute Myeloid Leukemia Cells by Targeting ATM]

Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2016 Apr;24(2):347-51. doi: 10.7534/j.issn.1009-2137.2016.02.008.
[Article in Chinese]


Objective: To investigate miR-181a function and regulation mechanism by identifying miR-181a target genes in acute myeloid leukemia (AML).

Methods: The HL-60 cells of human AML was transfected by small molecular analog miR-181a, the cell proliferation was detected by CCK-8 method after electroporation in HL-60 cell lines. Target genes of miR-181a were predicted and analyzed by the bioinformatics software and database. Target genes were confirmed by HL-60 cell line and the patient leukemia cells.

Results: Overexpressed miR-181a in HL-60 cell line significantly enhanced cell proliferation compared with that in control (P < 0.05). Dual luciferase reporter gene assay showed that miR-181a significantly suppressed the reporter gene activity containing ATM 3'-UTR by about 56.8% (P < 0.05), but it didn't suppress the reporter gene activity containing 3'-UTR ATM mutation. Western blot showed that miR-181a significantly downregulated the expression of ATM in human leukemia cells. It is also found that miR-181a was significantly increased in AML, which showed a negative correlation with ATM expression.

Conclusion: miR-181a promotes cell proliferation in AML by regulating the tumor suppressor ATM, thus it plays the role as oncogene in pathogenesis of AML.

MeSH terms

  • Ataxia Telangiectasia Mutated Proteins / metabolism*
  • Cell Proliferation*
  • Down-Regulation
  • HL-60 Cells
  • Humans
  • Leukemia, Myeloid, Acute / metabolism
  • Leukemia, Myeloid, Acute / pathology*
  • MicroRNAs / genetics
  • MicroRNAs / metabolism*
  • Transfection


  • MIrn181 microRNA, human
  • MicroRNAs
  • ATM protein, human
  • Ataxia Telangiectasia Mutated Proteins