MiRNA-485-5p suppresses the proliferation of acute myeloid leukemia via targeting SALL4

Eur Rev Med Pharmacol Sci. 2019 Jun;23(11):4842-4849. doi: 10.26355/eurrev_201906_18071.

Abstract

Objective: To examine the expression level of microRNA-485-5p (miRNA-485-5p) in acute myeloid leukemia (AML) and its biological function in regulating the proliferative ability of AML through targeting SALL4.

Patients and methods: Serum level of miRNA-485-5p in AML patients and healthy controls was determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). MiRNA-485-5p level in AML cell lines was detected by qRT-PCR as well. Proliferative and apoptotic changes in AML5 and U937 cells overexpressing miRNA-485-5p were assessed. Subsequently, the regulatory effect of miRNA-485-5p on SALL4 level was evaluated. Rescue experiments were conducted to uncover the role of miRNA-485-5p/SALL4 regulatory loop in regulating cellular behaviors of AML.

Results: Compared with healthy controls, serum level of miRNA-485-5p was lower in AML patients. MiRNA-485-5p was similarly downregulated in AML cell lines. Overexpression of miRNA-485-5p stimulated proliferation and alleviated apoptosis in AML. SALL4 level was downregulated by transfection of miRNA-485-5p mimics in AML5 and U937 cells. Overexpression of SALL4 could reverse the regulatory effect of miRNA-485-5p on proliferative and apoptotic abilities of AML.

Conclusions: MiRNA-485-5p is downregulated in AML. Overexpression of miRNA-485-5p alleviates the malignant progression of AML through downregulating SALL4.

MeSH terms

  • Apoptosis
  • Cell Proliferation
  • Cells, Cultured
  • Gene Expression Profiling
  • Humans
  • Leukemia, Myeloid, Acute / genetics
  • Leukemia, Myeloid, Acute / metabolism*
  • Leukemia, Myeloid, Acute / pathology*
  • MicroRNAs / blood
  • MicroRNAs / genetics
  • MicroRNAs / metabolism*
  • Transcription Factors / genetics
  • Transcription Factors / metabolism*

Substances

  • MIRN485 microRNA, human
  • MicroRNAs
  • SALL4 protein, human
  • Transcription Factors