scholarly journals Transformation of mouse BALB/c 3T3 cells with human basic fibroblast growth factor cDNA.

1988 ◽  
Vol 8 (2) ◽  
pp. 588-594 ◽  
Author(s):  
R Sasada ◽  
T Kurokawa ◽  
M Iwane ◽  
K Igarashi
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Cellular Transformation ◽  
Soft Agar ◽  
Transformed Cells ◽  
Fibroblast Growth ◽  
Morphological Transformation ◽  
Phenotypic Alteration ◽  
Autocrine Stimulation

The expression of human basic fibroblast growth factor (bFGF) cDNA in mouse BALB/c 3T3 clone A31 cells induced morphological transformation. These transformed cells grew well and reached more than a sixfold-higher saturation density than parental A31 cells even in serum-free medium. They were able to form colonies in soft agar. The phenotypic alteration in the transformed cells was reversed by the addition of anti-human bFGF antibodies to the medium. These results suggest that the cellular transformation mediated by bFGF is caused by autocrine stimulation with secreted bFGF molecules.

Transformation of mouse BALB/c 3T3 cells with human basic fibroblast growth factor cDNA

1988 ◽  
Vol 8 (2) ◽  
pp. 588-594
Author(s):  
R Sasada ◽  
T Kurokawa ◽  
M Iwane ◽  
K Igarashi
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Cellular Transformation ◽  
Soft Agar ◽  
Transformed Cells ◽  
Fibroblast Growth ◽  
Morphological Transformation ◽  
Phenotypic Alteration ◽  
Autocrine Stimulation

The expression of human basic fibroblast growth factor (bFGF) cDNA in mouse BALB/c 3T3 clone A31 cells induced morphological transformation. These transformed cells grew well and reached more than a sixfold-higher saturation density than parental A31 cells even in serum-free medium. They were able to form colonies in soft agar. The phenotypic alteration in the transformed cells was reversed by the addition of anti-human bFGF antibodies to the medium. These results suggest that the cellular transformation mediated by bFGF is caused by autocrine stimulation with secreted bFGF molecules.

scholarly journals Expression of human basic fibroblast growth factor cDNA in baby hamster kidney-derived cells results in autonomous cell growth.

1988 ◽  
Vol 106 (4) ◽  
pp. 1385-1394 ◽  
Author(s):  
G Neufeld ◽  
R Mitchell ◽  
P Ponte ◽  
D Gospodarowicz
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Constitutive Expression ◽  
Human Tumor ◽  
Soft Agar ◽  
Biologically Active ◽  
Fibroblast Growth ◽  
Baby Hamster Kidney ◽  
High Concentration

Growth factor over-production by responsive cells might contribute to their autonomous proliferation as well as their acquisition of a transformed phenotype in culture. Basic fibroblast growth factor (bFGF) has been shown to induce transient changes in cell behavior that resemble those encountered in transformed cells. In addition, several types of human tumor cells have been shown to produce bFGF. To determine directly the role that bFGF might play in the induction of the transformed phenotype, we have introduced a human bFGF cDNA expression vector into baby hamster kidney-derived (BHK-21) fibroblasts. One of the BHK transfectants, termed clone 19, expresses the bFGF mRNA and produces biologically active bFGF that accumulates to a high concentration inside the cells. These properties correlate with the ability of the cells to grow in serum-free medium without the addition of exogenous bFGF. Clone 19 cells also proliferated in soft agar, indicating that constitutive expression of the bFGF gene results in a loss of anchorage-dependent growth.

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.

scholarly journals Potential oncogenic effects of basic fibroblast growth factor requires cooperation between CUG and AUG-initiated forms.

1991 ◽  
Vol 2 (9) ◽  
pp. 709-718 ◽  
Author(s):  
B Couderc ◽  
H Prats ◽  
F Bayard ◽  
F Amalric
Keyword(s):  
Endothelial Cells ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Constitutive Expression ◽  
Soft Agar ◽  
Fibroblast Growth ◽  
Aortic Endothelial Cells ◽  
Tumorigenic Potential ◽  
Cell Immortalization

Normal adult bovine aortic endothelial cells were infected with various recombinant retroviruses expressing one, two, or three human basic fibroblast growth factor (bFGF) proteins normally synthesized by an alternative use of translation initiation codons. We show here that the constitutive expression of the AUG-initiated from (18 kDa) leads the transfected cells to form colonies in soft agar. The expression of the high molar weight (HMW) forms (22.5 and 21 kDa) initiated at one of the two CUG initiation codons allows cell immortalization, whereas the tumorigenic potential is reached when the three forms are constitutively expressed. Furthermore, we provide evidence that constitutive expression of (HMW) bFGF forms has a down-regulation effect on bFGF synthesis from the gene naturally active in parental endothelial cells.

A Case of Contact Dermatitis due to Fiblast Spray, a Product of Basic Fibroblast Growth Factor

2006 ◽  
Vol 68 (3) ◽  
pp. 248-250 ◽  
Author(s):  
Shuko OKADA ◽  
Takashi MASU ◽  
Takahiko TSUNODA ◽  
Ryuhei OKUYAMA ◽  
Setsuya AIBA
Keyword(s):  
Contact Dermatitis ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Fibroblast Growth
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