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The RNA Binding Protein IMP2 Preserves Glioblastoma Stem Cells by Preventing let-7 Target Gene Silencing

Nils Degrauwe1, Tommy B Schlumpf2, Michalina Janiszewska3

  • 1Division of Experimental Pathology, Institute of Pathology, CHUV, Faculty of Biology and Medicine, University of Lausanne, Rue du Bugnon 25, 1011 Lausanne, Switzerland.

Cell Reports
|May 18, 2016
PubMed

Insights

Glioblastoma stem cells (GSCs) maintain stemness through a LIN28-independent pathway. Insulin-like growth factor 2 mRNA-binding protein 2 (IMP2) prevents let-7 microRNA silencing, supporting GSC and neural stem cell growth.

Area of Science:

  • Molecular Biology
  • Developmental Biology
  • Cancer Research

Background:

  • Cancer stem cells (CSCs) drive tumor growth and rely on post-transcriptional gene regulation.
  • MicroRNAs (miRNAs), particularly the let-7 family, induce differentiation by silencing stem cell programs.
  • LIN28A/B proteins prevent let-7 biogenesis, maintaining stemness in embryonic and some cancer stem cells.

Purpose of the Study:

  • To investigate the mechanism of LIN28-independent let-7 silencing protection in glioblastoma stem cells (GSCs).
  • To identify factors that maintain stemness in GSCs despite the presence of let-7 and its target genes.

Main Methods:

  • Photoactivatable-ribonucleoside-enhanced crosslinking and immunoprecipitation (PAR-CLIP) to identify RNA-binding proteins.
  • Analysis of let-7 miRNA and target gene expression in GSCs.
  • Investigation of the role of insulin-like growth factor 2 mRNA-binding protein 2 (IMP2) in let-7 regulation.

Main Results:

  • Glioblastoma stem cells (GSCs) lack LIN28 but express let-7 and its target genes.
  • Insulin-like growth factor 2 mRNA-binding protein 2 (IMP2) binds to let-7 miRNA recognition elements (MREs).
  • IMP2 binding prevents let-7-mediated silencing of target genes, thus supporting stemness.

Conclusions:

  • Glioblastoma stem cells (GSCs) utilize a LIN28-independent mechanism to maintain stemness.
  • IMP2 plays a crucial role in protecting GSCs from let-7-mediated differentiation.
  • This mechanism is also relevant for neural stem cell specification.

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