miR-141-3p and TRAF5 Network Contributes to the Progression of T-Cell Acute Lymphoblastic Leukemia

Cell Transplant. 2019 Dec;28(1_suppl):59S-65S. doi: 10.1177/0963689719887370. Epub 2019 Nov 14.

Abstract

Numerous lines of evidence have shown that microRNAs (miRNAs) play a vital role in regulating the progression in many types of cancers, including T cell acute lymphoblastic leukemia (T-ALL). In this study, the potential underlying mechanism and functional role of miR-141-3p in T-ALL cells were determined. We found that the expression level of miR-141-3p was significantly downregulated, while that of tumor necrosis factor receptor-associated factor 5 (TRAF5) was strongly upregulated in tissues from patients with T-ALL compared with healthy controls. Subsequently, upregulation of miR-141-3p significantly repressed T-ALL cell proliferation and promoted cell apoptosis. Conversely, downregulation of miR-141-3p significantly inhibited cell apoptosis and enhanced T-ALL cell proliferation. We also verified that TRAF5 was the direct target of miR-141-3p in T-ALL cells. Additionally, TRAF5 overexpression significantly repressed cell apoptosis and increased T-ALL cell proliferation. In summary, miR-141-3p regulates T-ALL cell progression by directly targeting TRAF5, and may serve as a potential therapeutic target for T-ALL.

Keywords: T cells; T-ALL; TRAF5; apoptosis; miR-141-3p; proliferation.

MeSH terms

  • Adolescent
  • Apoptosis / genetics
  • Cell Line, Tumor
  • Cell Proliferation / genetics
  • Child
  • Child, Preschool
  • Disease Progression
  • Down-Regulation
  • Gene Silencing
  • Humans
  • Infant
  • MicroRNAs / genetics
  • MicroRNAs / metabolism*
  • Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / metabolism*
  • T-Lymphocytes / metabolism*
  • TNF Receptor-Associated Factor 5 / genetics
  • TNF Receptor-Associated Factor 5 / metabolism*
  • Up-Regulation

Substances

  • MIRN141 microRNA, human
  • MicroRNAs
  • TNF Receptor-Associated Factor 5
  • TRAF5 protein, human