scholarly journals Selective expression of high molecular weight basic fibroblast growth factor confers a unique phenotype to NIH 3T3 cells.

1991 ◽  
Vol 2 (9) ◽  
pp. 699-708 ◽  
Author(s):  
N Quarto ◽  
D Talarico ◽  
R Florkiewicz ◽  
D B Rifkin
Keyword(s):  
Molecular Weight ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
High Molecular Weight ◽  
Basic Fibroblast Growth Factor ◽  
Fibroblast Growth ◽  
3T3 Cells ◽  
Low Levels ◽  
Nih 3T3 ◽  
Nih 3T3 Cells

The phenotypes of NIH 3T3 cells transfected with basic fibroblast growth factor (bFGF) cDNAs that express only the high molecular weight (HMW) forms of bFGF, the 18-kDa form, or all forms were examined. Cells producing the 18 kDa or all forms of bFGF were transformed at high levels of growth factor expression but were nontransformed at low levels. Cell producing low levels of HMW forms of bFGF were growth impaired when compared with the parental cells. These cells tended to form multinucleated giant cells, did not grow in soft agar, were nontumorigenic, had a normal bFGF receptor number, and had a nontransformed morphology. Cells expressing high levels of HMW bFGFs had a transformed morphology and were tumorigenic. These data suggest a specific functional role for HMWbFGF.

scholarly journals Transformation of NIH 3T3 cells with basic fibroblast growth factor or the hst/K-fgf oncogene causes downregulation of the fibroblast growth factor receptor: reversal of morphological transformation and restoration of receptor number by suramin.

1989 ◽  
Vol 109 (5) ◽  
pp. 2519-2527 ◽  
Author(s):  
D Moscatelli ◽  
N Quarto
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Fibroblast Growth ◽  
3T3 Cells ◽  
Morphological Transformation ◽  
Normal Number ◽  
Receptor Number ◽  
Nih 3T3 ◽  
Nih 3T3 Cells

When NIH 3T3 cells were transfected with the cDNA for basic fibroblast growth factor (bFGF), most cells displayed a transformed phenotype. Acquisition of a transformed phenotype was correlated with the expression of high levels of bFGF (Quarto et al., 1989). Cells that had been transformed as a result of transfection with bFGF cDNA had a decreased capacity to bind 125I-bFGF to high affinity receptors. NIH 3T3 cells transfected with bFGF cDNA that expressed lower levels of bFGF were not transformed and had a normal number of bFGF receptors. NIH 3T3 cells transfected with the hst/Kfgf oncogene, which encodes a secreted molecule with 45% homology to bFGF, also displayed a transformed phenotype and decreased numbers of bFGF receptors. However, NIH 3T3 cells transfected with the H-ras oncogene were transformed but had a normal number of bFGF receptors. Thus, transformation by bFGF-like molecules resulted in downregulation of bFGF receptors. Receptor number was not affected by cell density for both parental NIH 3T3 cells and transformed cells. In the cells transfected with bFGF cDNA that were not transformed, the receptors could be downregulated in response to exogenous bFGF. Conditioned medium from transformed transfected cells contained sufficient quantities of bFGF to downregulate bFGF receptors on parental NIH 3T3 cells. Thus, the downregulation of bFGF receptors seemed related to the presence of bFGF in an extracytoplasmic compartment. Treatment of the transformed transfected NIH 3T3 cells with suramin, which blocks the interaction of bFGF with its receptor, reversed the morphological transformation and restored receptors almost to normal numbers. These results demonstrate that in these cells bFGF transforms cells by interacting with its receptor and that bFGF and hst/K-fgf may use the same receptor.

Species-Specific High Molecular Weight Forms of Basic Fibroblast Growth Factor

1990 ◽  
Vol 4 (1) ◽  
pp. 45-52 ◽  
Author(s):  
David R. Brigstock ◽  
Michael Klagsbrun ◽  
Joachim Sasse ◽  
Patricia A. Farber ◽  
Niggi Iberg
Keyword(s):  
Molecular Weight ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
High Molecular Weight ◽  
Basic Fibroblast Growth Factor ◽  
Fibroblast Growth ◽  
Species Specific

scholarly journals Fibroblast growth factor-1 stimulation of quiescent NIH 3T3 cells increases G/T mismatch-binding protein expression

1996 ◽  
Vol 319 (1) ◽  
pp. 9-12 ◽  
Author(s):  
Patrick J. DONOHUE ◽  
Sheau-Line Y. FENG ◽  
Gregory F ALBERTS ◽  
Yan GUO ◽  
Kimberly A PEIFLEY ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Binding Protein ◽  
Calf Serum ◽  
Mrna Levels ◽  
Fibroblast Growth ◽  
3T3 Cells ◽  
Nih 3T3 ◽  
Nih 3T3 Cells

Polypeptide growth factors promote cell-cycle progression in part by the transcriptional activation of a diverse group of specific genes. We have used an mRNA differential-display approach to identify several fibroblast growth factor (FGF)-1 (acidic FGF)-inducible genes in NIH 3T3 cells. Here we report that one of these genes, called FGF-regulated (FR)-3, is predicted to encode G/T mismatch-binding protein (GTBP), a component of the mammalian DNA mismatch correction system. The murine GTBP gene is transiently expressed after FGF-1 or calf serum treatment, with maximal mRNA levels detected at 12 and 18 h post-stimulation. FGF-1-stimulated NIH 3T3 cells also express an increased amount of GTBP as determined by immunoblot analysis. These results indicate that elevated levels of GTBP may be required during the DNA synthesis phase of the cell cycle for efficient G/T mismatch recognition and repair.

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