The role of C-Fos in growth factor regulation of stromelysin/transin gene expression.

L. D. Kerr, B. E. Magun, L. M. Matrisian

Research output: Contribution to journalArticlepeer-review

12 Scopus citations

Abstract

Expression of the rat stromelysin (transin) gene is stimulated by growth factors such as epidermal growth factor (EGF) and platelet-derived growth factor (PDGF), and inhibited by transforming growth factor-beta (TGF beta). Stimulation by both EGF and PDGF requires the presence of factors that recognize the AP-1 binding site in the stromelysin promoter, but PDGF stimulation requires induction of the protooncogene c-fos, while EGF acts through a FOS-independent pathway. The FOS-independent pathway appears to involve protein kinase C (PKC), since EGF, but not PDGF, requires activated protein kinase C to stimulate stromelysin expression. TGF beta inhibition of stromelysin gene expression requires an upstream sequence, referred to as the TGF beta inhibitory element (TIE). FOS is also a part of a protein complex that binds to the TIE. The protooncogene FOS is therefore involved in both stimulation and inhibition of stromelysin gene expression.

Original languageEnglish (US)
Pages (from-to)176-183
Number of pages8
JournalMatrix (Stuttgart, Germany). Supplement
Volume1
StatePublished - 1992

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