Limited miR-17-92 overexpression drives hematologic malignancies

Leuk Res. 2015 Mar;39(3):335-41. doi: 10.1016/j.leukres.2014.12.002. Epub 2014 Dec 10.

Abstract

The overexpression of microRNA cluster miR-17-92 has been implicated in development of solid tumors and hematological malignancies. The role of miR-17-92 in lymphomagenesis has been extensively investigated; however, because of the developmental defects caused by miR-17-92 dysregulation, its ability to drive tumorigenesis has remained undetermined until recently. Here we demonstrate that overexpression of miR-17-92 in a limited number of hematopoietic cells is sufficient to cause B cell malignancies. In sum, our study provides a novel and physiologically relevant model that exposes the potent ability of miR-17-92 to act as a driver of tumorigenesis.

Keywords: Lymphoma; Mouse model; miR-17-92.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Blotting, Western
  • Cell Proliferation
  • Cell Transformation, Neoplastic / pathology*
  • Gene Expression Regulation, Neoplastic*
  • Hematologic Neoplasms / genetics
  • Hematologic Neoplasms / metabolism
  • Hematologic Neoplasms / pathology*
  • Immunoenzyme Techniques
  • Integrases / metabolism
  • Mice
  • MicroRNAs / physiology*
  • Microfilament Proteins / physiology*
  • Muscle Proteins / physiology*
  • RNA, Messenger / genetics
  • Real-Time Polymerase Chain Reaction
  • Reverse Transcriptase Polymerase Chain Reaction
  • Tumor Cells, Cultured

Substances

  • MIRN17-92 microRNA, mouse
  • MicroRNAs
  • Microfilament Proteins
  • Muscle Proteins
  • RNA, Messenger
  • Tagln protein, mouse
  • Cre recombinase
  • Integrases