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Updated: Sep 26, 2026

Establishment of Epstein-Barr Virus Growth-transformed Lymphoblastoid Cell Lines
06:38

Establishment of Epstein-Barr Virus Growth-transformed Lymphoblastoid Cell Lines

Published on: November 8, 2011

Epstein-Barr virus antagonizes the antiproliferative activity of transforming growth factor-beta but does not abolish

Manuela Horndasch1, Eva E Raschke, Guido Bommer

  • 1Institute of Clinical Molecular Biology and Tumor Genetics, GSF-Research Center for Environment and Health, Munich, Germany.

International Journal of Cancer
|September 7, 2002
PubMed

Insights

Epstein-Barr virus (EBV) confers resistance to TGF-beta

Area of Science:

  • Molecular Biology
  • Virology
  • Immunology

Background:

  • Transforming growth factor-beta (TGF-beta) typically induces apoptosis and inhibits proliferation in B-lymphoma cells.
  • Epstein-Barr virus (EBV) immortalization confers resistance to TGF-beta's antiproliferative and proapoptotic effects in B cells.

Purpose of the Study:

  • To investigate the mechanism by which EBV overcomes TGF-beta-mediated growth arrest in B cells.
  • To determine if EBV interferes with the core TGF-beta signaling pathway.

Main Methods:

  • Generation of a lymphoblastoid cell line with an inducible EBV-specific transcriptional program (driven by EBNA2).
  • Assessment of TGF-beta responsiveness and target gene induction in EBV-expressing versus EBV-negative cells.

Main Results:

  • EBV-immortalized cells expressing the EBNA2-driven phenotype are resistant to TGF-beta-induced growth arrest.
  • EBV-driven cells remain responsive to TGF-beta, as evidenced by the induction of TGF-beta target genes.
  • EBV overcomes TGF-beta's antiproliferative activity without disrupting the core TGF-beta signaling pathway.

Conclusions:

  • EBV confers resistance to TGF-beta-mediated growth arrest in B cells.
  • This resistance is achieved without interfering with the fundamental TGF-beta signaling cascade.
  • EBV's mechanism of overcoming TGF-beta antiproliferative effects lies downstream of target gene induction.

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