Control of junB and extracellular matrix protein expression by transforming growth factor-β1 is independent of simian virus 40 T antigen-sensitive growth-inhibitory events Journal Article


Authors: Laiho, M.; Rönnstrand, L.; Heino, J.; Decaprio, J. A.; Ludlow, J. W.; Livingston, D. M.; Massagué, J.
Article Title: Control of junB and extracellular matrix protein expression by transforming growth factor-β1 is independent of simian virus 40 T antigen-sensitive growth-inhibitory events
Abstract: Treatment of Mv1Lu mink lung epithelial cells with transforming growth factor-β1 (TGF-β1) prevents phosphorylation of the retinoblastoma susceptibility gene product, RB, in late G1 phase of the cell cycle, which is thought to retain RB in a growth-suppressive state. This effect is paralleled by cell cycle arrest in late G1 (M. Laiho, J. A. DeCaprio, J. W. Ludlow, D. M. Livingston, and J. Massagué, Cell 62:175-185, 1990). Arrest can be prevented by expression of simian virus 40 T antigen, which binds to underphosphorylated RB, presumably blocking its growth-suppressive activity. The response of cells to TGF-β1, however, is complex and includes changes in the levels of expression of genes encoding nuclear transcription factors and extracellular matrix components. To define the relationships among various components of the TGF-β1 response, we have investigated the effect of TGF-β1 on cells whose growth-inhibitory response to this factor is prevented by T antigen. TGF-β1 addition to exponentially growing Mv1Lu cells increased the levels of junB mRNA and of three extracellular matrix proteins: plasminogen activator inhibitor-1, fibronectin, and thrombospondin. Kinetically, the effects on junB and plasminogen activator inhibitor-1 expression occurred faster (half-maximal at 1 to 2 h) than the effects on fibronectin and thrombospondin expression (half-maximal at 6 to 10 h). These effects either preceded or overlapped, respectively, the withdrawal of Mv1Lu cells from the cell cycle. Expression of a transfected T-antigen gene in Mv1Lu cells, however, did not prevent any of these responses to TGF-β1. The results indicate that TGF-β1-stimulated expression of junB and extracellular matrix proteins in Mv1Lu cells can occur independently of the T-antigen-sensitive events that lead to growth arrest.
Keywords: dna-binding proteins; nonhuman; animal cell; animal; mammalia; cell cycle; gene expression; transforming growth factor beta; cell line; transfection; animalia; extracellular matrix; gene expression regulation; rna, messenger; mammal; lung; virus large t antigen; simian virus 40; mink; growth inhibition; thrombospondins; fibronectins; simiae; genes, retinoblastoma; proto-oncogene proteins c-jun; simian virus; priority journal; article; support, non-u.s. gov't; support, u.s. gov't, p.h.s.; support, u.s. gov't, non-p.h.s.; oncogene c jun; mustela vison; plasminogen inactivators; platelet membrane glycoproteins
Journal Title: Molecular and Cellular Biology
Volume: 11
Issue: 2
ISSN: 0270-7306
Publisher: American Society for Microbiology  
Date Published: 1991-02-01
Start Page: 972
End Page: 978
Language: English
PUBMED: 1990295
PROVIDER: scopus
PMCID: PMC359761
DOI: 10.1128/mcb.11.2.972
DOI/URL:
Notes: Jkrki Heino's first name is misspelled on the original publication -- Source: Scopus
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  1. Joan Massague
    389 Massague
  2. Marikki Laiho
    12 Laiho