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MicroRNA-142-3p inhibits cell proliferation in human acute lymphoblastic leukemia by targeting the MLL-AF4 oncogene

Liping Dou1, Jingxin Li, Dehua Zheng

  • 1Department of Hematology, Chinese PLA General Hospital, Fuxing Road 28th, Beijing, 100853, China.

Molecular Biology Reports
|September 24, 2013
PubMed

Insights

MicroRNA-142-3p acts as a tumor suppressor in acute lymphoblastic leukemia (ALL) with the MLL-AF4 fusion protein. Upregulating this microRNA inhibits cancer cell growth and promotes cell death by targeting MLL-AF4.

Area of Science:

  • Molecular Biology
  • Oncology
  • Genetics

Background:

  • The MLL-AF4 fusion protein, resulting from t(4;11) translocation, is associated with poor prognosis in acute lymphoblastic leukemia (ALL).
  • Mechanisms regulating MLL-AF4 expression in ALL are not fully understood.

Purpose of the Study:

  • To investigate the role of microRNA-142-3p (miR-142-3p) in the regulation of MLL-AF4 expression in ALL.
  • To determine the functional impact of miR-142-3p on MLL-AF4-positive ALL cells.

Main Methods:

  • Quantitative analysis of miR-142-3p levels in ALL patients.
  • In vitro experiments using the RS4;11 leukemic cell line to assess the effects of miR-142-3p modulation on MLL-AF4 expression, cell proliferation, and apoptosis.
  • Analysis of MLL-AF4 target gene expression.

Main Results:

  • miR-142-3p was significantly downregulated in ALL patients with MLL-AF4.
  • Upregulation of miR-142-3p in RS4;11 cells reduced MLL-AF4 expression, suppressed proliferation, and induced apoptosis.
  • miR-142-3p directly targets MLL-AF4 and represses its downstream targets, including HOXA9, HOXA7, and HOXA10.

Conclusions:

  • miR-142-3p functions as a tumor suppressor in MLL-AF4-positive ALL.
  • The growth-suppressive effects of miR-142-3p are primarily mediated by the repression of MLL-AF4 expression and its target genes.

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