A Probabilistic Boolean Network Approach for the Analysis of Cancer-Specific Signalling: A Case Study of Deregulated PDGF Signalling in GIST

PLoS One. 2016 May 27;11(5):e0156223. doi: 10.1371/journal.pone.0156223. eCollection 2016.

Abstract

Background: Signal transduction networks are increasingly studied with mathematical modelling approaches while each of them is suited for a particular problem. For the contextualisation and analysis of signalling networks with steady-state protein data, we identified probabilistic Boolean network (PBN) as a promising framework which could capture quantitative changes of molecular changes at steady-state with a minimal parameterisation.

Results and conclusion: In our case study, we successfully applied the PBN approach to model and analyse the deregulated Platelet-Derived Growth Factor (PDGF) signalling pathway in Gastrointestinal Stromal Tumour (GIST). We experimentally determined a rich and accurate dataset of steady-state profiles of selected downstream kinases of PDGF-receptor-alpha mutants in combination with inhibitor treatments. Applying the tool optPBN, we fitted a literature-derived candidate network model to the training dataset consisting of single perturbation conditions. Model analysis suggested several important crosstalk interactions. The validity of these predictions was further investigated experimentally pointing to relevant ongoing crosstalk from PI3K to MAPK signalling in tumour cells. The refined model was evaluated with a validation dataset comprising multiple perturbation conditions. The model thereby showed excellent performance allowing to quantitatively predict the combinatorial responses from the individual treatment results in this cancer setting. The established optPBN pipeline is also widely applicable to gain a better understanding of other signalling networks at steady-state in a context-specific fashion.

MeSH terms

  • Computational Biology / methods*
  • Gastrointestinal Stromal Tumors / genetics
  • Gastrointestinal Stromal Tumors / pathology*
  • Humans
  • MAP Kinase Signaling System
  • Platelet-Derived Growth Factor / metabolism*
  • Point Mutation
  • Probability
  • Signal Transduction*

Substances

  • Platelet-Derived Growth Factor

Grants and funding

This work was supported by the grants F1R-LSC-PUL-09PDGF and F1R-LSC-PUL-11PDGF of the University of Luxembourg. Panuwat Trairatphisan is a recipient of fellowships allocated by the Fonds National de la Recherche Luxembourg (AFR grant number 1233900). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.