PMID- 1990295 OWN - NLM STAT- MEDLINE DCOM- 19910304 LR - 20210526 IS - 0270-7306 (Print) IS - 1098-5549 (Electronic) IS - 0270-7306 (Linking) VI - 11 IP - 2 DP - 1991 Feb TI - 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. PG - 972-8 AB - 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. FAU - Laiho, M AU - Laiho M AD - Howard Hughes Medical Institute, Memorial Sloan-Kettering Cancer Center, New York, New York 10021. FAU - Ronnstrand, L AU - Ronnstrand L FAU - Heino, J AU - Heino J FAU - Decaprio, J A AU - Decaprio JA FAU - Ludlow, J W AU - Ludlow JW FAU - Livingston, D M AU - Livingston DM FAU - Massague, J AU - Massague J LA - eng GR - CA 34610/CA/NCI NIH HHS/United States GR - CA 39240/CA/NCI NIH HHS/United States GR - CA 50661/CA/NCI NIH HHS/United States PT - Journal Article PT - Research Support, Non-U.S. Gov't PT - Research Support, U.S. Gov't, Non-P.H.S. PT - Research Support, U.S. Gov't, P.H.S. PL - United States TA - Mol Cell Biol JT - Molecular and cellular biology JID - 8109087 RN - 0 (DNA-Binding Proteins) RN - 0 (Fibronectins) RN - 0 (Plasminogen Inactivators) RN - 0 (Platelet Membrane Glycoproteins) RN - 0 (Proto-Oncogene Proteins c-jun) RN - 0 (RNA, Messenger) RN - 0 (Thrombospondins) RN - 0 (Transforming Growth Factor beta) SB - IM MH - Animals MH - Cell Cycle MH - Cell Line MH - DNA-Binding Proteins/*genetics MH - Extracellular Matrix/*metabolism MH - Fibronectins/*genetics MH - Gene Expression Regulation MH - Genes, Retinoblastoma/drug effects MH - Lung MH - Mink MH - Plasminogen Inactivators/*metabolism MH - Platelet Membrane Glycoproteins/*genetics MH - Proto-Oncogene Proteins c-jun MH - RNA, Messenger/genetics/isolation & purification MH - Thrombospondins MH - Transfection MH - Transforming Growth Factor beta/*pharmacology PMC - PMC359761 EDAT- 1991/02/01 00:00 MHDA- 1991/02/01 00:01 PMCR- 1991/02/01 CRDT- 1991/02/01 00:00 PHST- 1991/02/01 00:00 [pubmed] PHST- 1991/02/01 00:01 [medline] PHST- 1991/02/01 00:00 [entrez] PHST- 1991/02/01 00:00 [pmc-release] AID - 10.1128/mcb.11.2.972-978.1991 [doi] PST - ppublish SO - Mol Cell Biol. 1991 Feb;11(2):972-8. doi: 10.1128/mcb.11.2.972-978.1991.