Modulation of JB6 mouse epidermal cell transformation response by the prostaglandin F receptor

Thomas J. Weber, Lye M. Markillie, William B. Chrisler, George A. Vielhauer, John W. Regan

Research output: Contribution to journalArticlepeer-review

9 Scopus citations


Prostaglandin F (PGF) modulates clonal selection processes in the mouse skin model of carcinogenesis. In this study we investigated whether JB6 mouse epidermal cells expressed a functional PGF receptor (FP) coupled with a cell-transformation response. Treatment of JB6 cells with an FP agonist (fluprostenol) potently (pM-nM) increased anchorage-dependent and anchorage-independent growth. Inositol phospholipid accumulation and extracellular signal-regulated kinase (Erk) activity were increased in cells treated with FP agonists, consistent with established FP- related signal transduction. FP mRNA was detected by reverse transcription-polymerase chain reaction, and the average specific [3H]PGF binding was 8.25 ± 0.95 fmol/mg protein. Erk activity and colony size were increased by cotreatment of JB6 cells with epidermal growth factor (EGF) and fluprostenol to a greater extent than with either treatment alone, whereas the cotreatment effect on colony number appeared to be simply additive. Collectively, our data indicated that JB6 cells expressed a functional FP coupled with transformation-related signal transduction and the regulation of clonal selection processes. Erk activity appears to be a convergence point in the EGF and FP pathways. The data raise the possibility that the FP contributes to clonal selection processes but probably plays a more important role as a response modifier.

Original languageEnglish (US)
Pages (from-to)163-172
Number of pages10
JournalMolecular Carcinogenesis
Issue number4
StatePublished - Dec 1 2002


  • Convergence
  • Cyclooxygenase
  • Epidermal
  • Extracellular signal-regulated kinase

ASJC Scopus subject areas

  • Molecular Biology
  • Cancer Research


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