Comparative expression study of the endo-G protein coupled receptor (GPCR) repertoire in human glioblastoma cancer stem-like cells, U87-MG cells and non malignant cells of neural origin unveils new potential therapeutic targets

PLoS One. 2014 Mar 24;9(3):e91519. doi: 10.1371/journal.pone.0091519. eCollection 2014.

Abstract

Glioblastomas (GBMs) are highly aggressive, invasive brain tumors with bad prognosis and unmet medical need. These tumors are heterogeneous being constituted by a variety of cells in different states of differentiation. Among these, cells endowed with stem properties, tumor initiating/propagating properties and particularly resistant to chemo- and radiotherapies are designed as the real culprits for tumor maintenance and relapse after treatment. These cells, termed cancer stem-like cells, have been designed as prominent targets for new and more efficient cancer therapies. G-protein coupled receptors (GPCRs), a family of membrane receptors, play a prominent role in cell signaling, cell communication and crosstalk with the microenvironment. Their role in cancer has been highlighted but remains largely unexplored. Here, we report a descriptive study of the differential expression of the endo-GPCR repertoire in human glioblastoma cancer stem-like cells (GSCs), U-87 MG cells, human astrocytes and fetal neural stem cells (f-NSCs). The endo-GPCR transcriptome has been studied using Taqman Low Density Arrays. Of the 356 GPCRs investigated, 138 were retained for comparative studies between the different cell types. At the transcriptomic level, eight GPCRs were specifically expressed/overexpressed in GSCs. Seventeen GPCRs appeared specifically expressed in cells with stem properties (GSCs and f-NSCs). Results of GPCR expression at the protein level using mass spectrometry and proteomic analysis are also presented. The comparative GPCR expression study presented here gives clues for new pathways specifically used by GSCs and unveils novel potential therapeutic targets.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Astrocytes / cytology
  • Astrocytes / pathology
  • Cell Differentiation
  • Cell Line, Tumor
  • Fetus / cytology
  • Fetus / metabolism
  • Fetus / pathology
  • Gene Expression Profiling*
  • Glioblastoma / drug therapy
  • Glioblastoma / genetics
  • Glioblastoma / metabolism
  • Glioblastoma / pathology*
  • Humans
  • Molecular Targeted Therapy*
  • Neoplastic Stem Cells / pathology*
  • Ploidies
  • Proteomics*
  • Receptors, G-Protein-Coupled / genetics*
  • Receptors, G-Protein-Coupled / metabolism*

Substances

  • Receptors, G-Protein-Coupled

Grants and funding

This work was supported by La Ligue contre le Cancer, La Fondation pour la Recherche Médicale, the Agence Nationale pour la Recherche (ANR), the Proteomic French Infrastructure (ANR-10-INSB-08-03), the Région Alsace, Université de Strasbourg, CNRS, the French Ministère de l'enseignement supérieur et de la recherche, the Fondation ARC (SFI20121205939, HC/MPJ) and has been preformed within the LABEX ANR-10-LABX-0034_Medalis and received a financial support from French government managed by “Agence National de la Recherche” under “Programme d'investissement d'avenir”. Marie Fève is indebted to French Ministère de l'enseignement supérieur et de la recherche for doctoral fellowship and Sarah Lennon to the Fondation ARC pour la Recherche sur le Cancer. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.