Changes in rasT24 expression do not induce changes in c‐jun, jun‐B, or jun‐D RNA levels in rat liver epithelial cells

David B. Krizman, Russell M. Lebovitz, Michael W. Lieberman

Research output: Contribution to journalArticlepeer-review

1 Scopus citations

Abstract

We used a series of rat liver epithelial (RLE) cell lines that carry a zinc-regulatable metallothionein/rasT24 fusion gene (MTrasT24) to investigate the relation of ras oncogene expression to steady-state RNA levels of the jun family of genes. In these cells, steady-state RNA levels of c-jun, jun-B, and jun-D were unrelated to rasT24 RNA levels or the phenotypic changes induced by the ras oncogene. Steady-state levels of the three jun mRNAs varied among different rasT24 transformed clones, and, although some clones exhibited concomitant induction of rasT24 and jun mRNAs, other clones exhibited no such correlation. We conclude that the effects of rasT24 in transformed RLE cells do not appear to be mediated by c-jun, jun-B, or jun-D and that studies examining only a single transformed clone may give misleading results with respect to the role of various oncogenes in the transformation process

Original languageEnglish (US)
Pages (from-to)264-267
Number of pages4
JournalMolecular Carcinogenesis
Volume3
Issue number5
DOIs
StatePublished - 1990

Keywords

  • Carcinogenesis
  • gene expression
  • oncogene
  • transformation

ASJC Scopus subject areas

  • Cancer Research
  • Molecular Biology

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