Volume 7 Supplement 2

13th Scientific Symposium of the Austrian Pharmacological Society (APHAR). Joint Meeting with the Austrian Society of Toxicology (ASTOX) and the Hungarian Society for Experimental and Clinical Pharmacology (MFT)

Open Access

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

  • Sandra Sagmeister1,
  • Maria Eisenbauer1,
  • Christine Pirker1,
  • Klaus Holzmann1,
  • Wolfram Parzefall1,
  • Christopher Gerner1,
  • Rolf Schulte-Hermann1 and
  • Bettina Grasl-Kraupp1Email author
BMC Pharmacology20077(Suppl 2):A59

DOI: 10.1186/1471-2210-7-S2-A59

Published: 14 November 2007

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.

Authors’ Affiliations

(1)
Department of Medicine I, Institute of Cancer Research, Medical University of Vienna

Copyright

© Sagmeister et al; licensee BioMed Central Ltd. 2007

This article is published under license to BioMed Central Ltd.

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