v-jun Oncogene Suppresses Both Phorbol Ester-induced Cell Invasion and Stromelysin Gene Expression in a Mouse Papilloma Cell Line

Tom C. Tsang, Yi Wen Chu, Marianne B. Powell, John Kittelson, Linda Meade-Tollin, Mary J.C. Hendrix, Tim Bowden*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

5 Scopus citations

Abstract

The viral jun (v-jun) oncogene encodes a transcription factor that can participate in the transactivation of genes through the AP-1 complex. Evidence indicates that the ability of v-jun to transform cells and stimulate transcription depends on the cell type. We have asked whether expression of the v-jun gene in benign tumor forming mouse keratinocytes that already express an activated c-rasHa oncogene would cause malignant progression. Our results showed that the v-jun transfection did not result in malignant progression; instead, we made the unexpected observation that the ability of these cells to invade reconstituted basement membrane matrix (in vitro) in response to the phorbol ester, 12-O-tetradecanoylphor-bol-13-acetate, was suppressed. This phenomenon could, in part, be explained by the suppression of the induction by phorbol ester of expression of the metalloproteinase, stromelysin (transin). Of interest was the Finding that 12-O-tetradecanoylphorbol-13-acetate induction of other cellular genes known to be regulated by AP-1 was not inhibited in the benign tumor cells expressing V-jun.

Original languageEnglish (US)
Pages (from-to)882-886
Number of pages5
JournalCancer Research
Volume54
Issue number4
StatePublished - Feb 1994

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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