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BMC Pharmacology

, 7:A59 | Cite as

New epithelial and mesenchymal cell lines from primary liver cancer to study cell interactions in hepatocarcinogenesis

  • Sandra Sagmeister
  • Maria Eisenbauer
  • Christine Pirker
  • Klaus Holzmann
  • Wolfram Parzefall
  • Christopher Gerner
  • Rolf Schulte-Hermann
  • Bettina Grasl-Kraupp
Open Access
Meeting abstract
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Keywords

Reactive Oxygen Species Liver Cancer Hepatocyte Growth Factor Human Hepatocellular Carcinoma Primary Liver Cancer 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

To study cell interactions in tumor development, new epithelial and mesenchymal cell lines were established from human hepatocellular carcinoma by spontaneous outgrowth in culture. We obtained several hepatocarcinoma (HCC), B-lymphoblastoid (BLC) and myofibroblastoid (MF) lines. In-depth characterization included cell kinetics, genotype, tumorigenicity, expression of cell-type specific markers and proteome patterns. Many functions of cells of origin were found to be preserved. Thus, HCC cells secrete albumin and α1-antitrypsin, BLC cells phagocytose and release TNF-β, other cytokines and reactive oxygen species upon stimulation, while MF cells express fibulin-2, vimentin and hepatocyte growth factor (HGF). We studied the impact of the mesenchymal lines on hepatocarcinogenesis by in vitro assays. BLC and MF supernatants strongly increased DNA replication of premalignant hepatocytes. The stimulation by MF lines was mainly attributed to HGF secretion. In HCC cells, MF supernatant had only minor effects on cell growth but enhanced migration. MF lines also stimulated neoangiogenesis via vEGF release. BLC supernatant induced dramatically death of HCC cells, which could be largely abrogated by neutralizing the supernatant with TNF-β-antiserum. In conclusion, the new cell lines reveal stage-specific stimulatory and inhibitory interactions between mesenchymal and epithelial tumor cells. They offer new tools to unravel the role of the microenvironment during hepatocarcinogenesis.

Copyright information

© Sagmeister et al; licensee BioMed Central Ltd. 2007

This article is published under license to BioMed Central Ltd.

Authors and Affiliations

  • Sandra Sagmeister
    • 1
  • Maria Eisenbauer
    • 1
  • Christine Pirker
    • 1
  • Klaus Holzmann
    • 1
  • Wolfram Parzefall
    • 1
  • Christopher Gerner
    • 1
  • Rolf Schulte-Hermann
    • 1
  • Bettina Grasl-Kraupp
    • 1
  1. 1.Department of Medicine I, Institute of Cancer ResearchMedical University of ViennaAustria

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