Tumourigenic characteristics of embryonal carcinoma cells as a model for studying tumour progression of human embryonic stem cells

Cell Prolif. 2012 Aug;45(4):299-310. doi: 10.1111/j.1365-2184.2012.00827.x.

Abstract

Objectives: The objective of this study was to compare tumourigenic characteristics of human embryonic stem cells (HESCs) and embryonal carcinoma cells (ECCs) to identify a robust and simple model for studying certain aspects of cell transformation and tumourigenesis, in tumour progression of HESCs.

Materials and methods: SSEA-3 positive ECCs (NTERA-2) cells were identified and compared to HESCs (ch HES-20) in terms of pluripotency and differentiation capacity, growth characteristics, gene expression profiles and signalling pathways.

Results: Our results showed that NTERA-2 cells shared similarities in expression markers of pluripotency to ch HES-20 cells. However, NTERA-2 cells also expressed some markers of differentiation and had a tendency to differentiate towards ectodermal endpoints. We identified NTERA-2 cells with higher S-phase fraction in cell cycle distribution, anti-apoptosis markers and robust self-renewal ability, compared to ch HES-20 cells. Microarray analysis and real-time PCR results showed that some oncogenes were up-regulated and tumour-suppression genes were down-regulated, whereas pluripotency-related genes were up-regulated and differentiation-related genes were down-regulated, and that Wnt and Notch signalling pathways were activated during progression from ES cells to EC cells.

Conclusion: Tumourigenic characteristics of ECCs may provide a valuable insight into possible tumour progression of HESCs.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis
  • Carcinoma, Embryonal / pathology*
  • Cell Differentiation
  • Cell Proliferation
  • Cell Transformation, Neoplastic
  • Disease Progression
  • Embryonic Stem Cells / cytology*
  • Flow Cytometry
  • Genes, Tumor Suppressor
  • Humans
  • Models, Biological*
  • Real-Time Polymerase Chain Reaction
  • Signal Transduction