Advanced

Control of junB and extracellular matrix protein expression by transforming growth factor-beta 1 is independent of simian virus 40 T antigen-sensitive growth-sensitive growth-inhibitory events

Laiho, Marikki; Rönnstrand, Lars LU ; Heino, Jyrki; DiCaprio, JA; Ludlow, JW; Livingston, DM and Massagué, Joan (1991) In Molecular and Cellular Biology 11(2). p.972-978
Abstract
Treatment of Mv1Lu mink lung epithelial cells with transforming growth factor-beta 1 (TGF-beta 1) 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. DeCapric, J. W. Ludlow, D. M. Livingston, and J. Massague, 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-beta 1, however, is complex and includes changes in the levels of expression of genes encoding nuclear transcription factors... (More)
Treatment of Mv1Lu mink lung epithelial cells with transforming growth factor-beta 1 (TGF-beta 1) 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. DeCapric, J. W. Ludlow, D. M. Livingston, and J. Massague, 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-beta 1, 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-beta 1 response, we have investigated the effect of TGF-beta 1 on cells whose growth-inhibitory response to this factor is prevented by T antigen. TGF-beta 1 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-beta 1. The results indcate that TGF-B1-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. (Less)
Please use this url to cite or link to this publication:
author
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Messenger/genetics/isolation & purification Thrombospondins Transfection Transforming Growth Factor beta/*pharmacology, Animals Cell Cycle Cell Line DNA-Binding Proteins/*genetics Extracellular Matrix/*metabolism Fibronectins/*genetics Gene Expression Regulation Genes, Retinoblastoma/drug effects Lung Mink Plasminogen Inactivators/*metabolism Platelet Membrane Glycoproteins/*genetics Proto-Oncogene Proteins c-jun RNA
in
Molecular and Cellular Biology
volume
11
issue
2
pages
972 - 978
publisher
American Society for Microbiology
ISSN
0270-7306
language
English
LU publication?
no
id
039e78a7-d4c4-4753-8f19-473ff9df33f1 (old id 1784205)
date added to LUP
2011-02-07 15:25:56
date last changed
2016-06-29 09:06:39
@article{039e78a7-d4c4-4753-8f19-473ff9df33f1,
  abstract     = {Treatment of Mv1Lu mink lung epithelial cells with transforming growth factor-beta 1 (TGF-beta 1) 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. DeCapric, J. W. Ludlow, D. M. Livingston, and J. Massague, 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-beta 1, 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-beta 1 response, we have investigated the effect of TGF-beta 1 on cells whose growth-inhibitory response to this factor is prevented by T antigen. TGF-beta 1 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-beta 1. The results indcate that TGF-B1-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.},
  author       = {Laiho, Marikki and Rönnstrand, Lars and Heino, Jyrki and DiCaprio, JA and Ludlow, JW and Livingston, DM and Massagué, Joan},
  issn         = {0270-7306},
  keyword      = {Messenger/genetics/isolation & purification
Thrombospondins
Transfection
Transforming Growth Factor beta/*pharmacology,Animals
Cell Cycle
Cell Line
DNA-Binding Proteins/*genetics
Extracellular Matrix/*metabolism
Fibronectins/*genetics
Gene Expression Regulation
Genes,Retinoblastoma/drug effects
Lung
Mink
Plasminogen Inactivators/*metabolism
Platelet Membrane Glycoproteins/*genetics
Proto-Oncogene Proteins c-jun
RNA},
  language     = {eng},
  number       = {2},
  pages        = {972--978},
  publisher    = {American Society for Microbiology},
  series       = {Molecular and Cellular Biology},
  title        = {Control of junB and extracellular matrix protein expression by transforming growth factor-beta 1 is independent of simian virus 40 T antigen-sensitive growth-sensitive growth-inhibitory events},
  volume       = {11},
  year         = {1991},
}