RNA-Seq Differentiates Tumour and Host mRNA Expression Changes Induced by Treatment of Human Tumour Xenografts with the VEGFR Tyrosine Kinase Inhibitor Cediranib

PLoS One. 2013 Jun 19;8(6):e66003. doi: 10.1371/journal.pone.0066003. Print 2013.

Abstract

Pre-clinical models of tumour biology often rely on propagating human tumour cells in a mouse. In order to gain insight into the alignment of these models to human disease segments or investigate the effects of different therapeutics, approaches such as PCR or array based expression profiling are often employed despite suffering from biased transcript coverage, and a requirement for specialist experimental protocols to separate tumour and host signals. Here, we describe a computational strategy to profile transcript expression in both the tumour and host compartments of pre-clinical xenograft models from the same RNA sample using RNA-Seq. Key to this strategy is a species-specific mapping approach that removes the need for manipulation of the RNA population, customised sequencing protocols, or prior knowledge of the species component ratio. The method demonstrates comparable performance to species-specific RT-qPCR and a standard microarray platform, and allowed us to quantify gene expression changes in both the tumour and host tissue following treatment with cediranib, a potent vascular endothelial growth factor receptor tyrosine kinase inhibitor, including the reduction of multiple murine transcripts associated with endothelium or vessels, and an increase in genes associated with the inflammatory response in response to cediranib. In the human compartment, we observed a robust induction of hypoxia genes and a reduction in cell cycle associated transcripts. In conclusion, the study establishes that RNA-Seq can be applied to pre-clinical models to gain deeper understanding of model characteristics and compound mechanism of action, and to identify both tumour and host biomarkers.

Publication types

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

MeSH terms

  • Animals
  • Carcinoma, Non-Small-Cell Lung / drug therapy*
  • Carcinoma, Non-Small-Cell Lung / genetics
  • Cell Cycle / drug effects
  • Cell Hypoxia / drug effects
  • Cell Line, Tumor
  • Computational Biology
  • Gene Expression Profiling / methods
  • Gene Expression Regulation, Neoplastic / drug effects
  • Gene Regulatory Networks / drug effects*
  • Humans
  • Lung Neoplasms / drug therapy*
  • Lung Neoplasms / genetics
  • Mice
  • Oligonucleotide Array Sequence Analysis / methods
  • Protein Kinase Inhibitors / administration & dosage*
  • Protein Kinase Inhibitors / pharmacology
  • Quinazolines / administration & dosage*
  • Quinazolines / pharmacology
  • Real-Time Polymerase Chain Reaction
  • Sequence Analysis, RNA / methods*
  • Species Specificity
  • Xenograft Model Antitumor Assays

Substances

  • Protein Kinase Inhibitors
  • Quinazolines
  • cediranib

Grants and funding

The work was funded by AstraZeneca (www.astrazeneca.com) who are current employers of JRB, SJP, SR, SLW, HB, OD, MW, NRS, THC, JRD and STB, and past employers of MF and NJG. Other than the named authors, the funder had no direct role in study design, data collection and analysis, decision to publish, and preparation of the manuscript.