Growth Regulation in Normal and Transformed Cells

Nature ◽  
1971 ◽  
Vol 232 (5311) ◽  
pp. 445-445
Keyword(s):  
Growth Regulation ◽  
Transformed Cells

Alteration of homeobox gene expression by N-ras transformation of PA-1 human teratocarcinoma cells

1991 ◽  
Vol 11 (7) ◽  
pp. 3573-3583
Author(s):  
R Buettner ◽  
S O Yim ◽  
Y S Hong ◽  
E Boncinelli ◽  
M A Tainsky
Keyword(s):  
Cell Differentiation ◽  
Growth Regulation ◽  
Homeobox Genes ◽  
Constitutive Expression ◽  
Homeobox Gene ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
Transformed Cells ◽  
Teratocarcinoma Cell ◽  
Cell Clones

We used a series of cell clones from a human teratocarcinoma cell line, PA-1, to study the effect of transformation by an activated N-ras oncogene on the expression of genes involved in retinoic acid (RA)-induced differentiation and growth regulation. Recently, it has been shown that expression of human HOX 2 genes is sequentially activated by RA beginning from Hox 2.9 at the 3' end of the HOX 2 cluster (A. Simeone, D. Acampora, L. Arcioni, P. W. Andrews, E. Boncinelli, and F. Mavilio, Nature [London] 346:763-766, 1990). We now report that six different genes of the cluster HOX 1 are sequentially induced by RA in a similar temporal pattern, beginning with genes at the 3' end of the cluster. However, in N-ras-transformed cell clones, RA-induced expression of these homeobox genes is delayed. Hox 1.4 and Hox 1.3, genes abundantly induced in nontransformed clones after 3 days of RA treatment, are expressed in N-ras-transformed cells only after 10 days of RA treatment. At this time, the cells' growth is arrested at very high density, and no differentiated morphologic characteristics are observed. Constitutive expression of a transfected Hox 1.4 gene under the control of a simian virus 40 promotor leads to differentiated cell morphology similar to that of the RA-induced phenotype and restores the growth-inhibitory effects of RA in N-ras-transformed cells. These observations provide evidence that enhanced proliferation in N-ras-transformed cells compromises teratocarcinoma cell differentiation by a mechanism that transiently suppresses homeobox gene induction and implies a central role for homeobox genes in RA-induced cell differentiation. We conclude that stimulation of a putative growth factor signal pathway, associated with ras-induced proliferation, transiently suppresses the induction of transcription factors functionally involved in cell growth and differentiation.

Anchorage and growth regulation in normal and virus-transformed cells

1968 ◽  
Vol 3 (5) ◽  
pp. 683-693 ◽  
Author(s):  
Michael Stoker ◽  
Charles O'Neill ◽  
Susan Berryman ◽  
Vivienne Waxman
Keyword(s):  
Growth Regulation ◽  
Transformed Cells

Transfer of Growth Inhibition Between Normal and Virus-Transformed Cells: Autoradiographic Studies Using Marked Cells

1967 ◽  
Vol 2 (3) ◽  
pp. 293-304
Author(s):  
M. G. P. STOKER
Keyword(s):  
Growth Inhibition ◽  
Mouse Embryo ◽  
Normal Mouse ◽  
Growth Regulation ◽  
Thymidine Incorporation ◽  
Mixed Cultures ◽  
Transformed Cells ◽  
Normal Cells ◽  
Embryo Cells ◽  
Marking Technique

[3H]Thymidine and [3H]hypoxanthine incorporation were investigated by autoradiography in mixed cultures of polyoma-transformed BHK21 cells and freshly isolated mouse fibroblasts, with ingested carbon or carmine granules as markers to distinguish the cells. An assessment of the marking technique showed that there was some exchange of granules in the mixed cultures which prevented certain identification of individual cells, but suitable criteria were chosen for distinguishing the cells on a statistical basis. Thymidine incorporation was inhibited in one third to two thirds of the transformed cells when they were in contact with stationary layers of normal cells, which themselves showed a low proportion with thymidine incorporation. Transformed cells in the same dish which were not touching the normal cells showed no inhibition of thymidine incorporation. This is in agreement with the earlier observation that growth of transformed BHK21 cells is inhibited by contact with stationary normal fibroblasts. Experiments were also carried out on hypoxanthine incorporation with the TG1 variant of polyoma-transformed cells. TG1 cells are deficient in inosinic pyrophosphorylase and autoradiography shows a failure to incorporate hypoxanthine. When TG1 cells were cultured in contact with normal mouse embryo cells, however, it was found that hypoxanthine was present in the TG1 cells as well as in the normal cells. Increased incorporation did not occur in TG1 cells in the same dish which were not in contact with normal cells. This confirms earlier observations and shows that certain substances can pass directly from normal to transformed cells. It suggests the possibility that molecules concerned in growth regulation might also be transferred directly between contiguous cells.

scholarly journals Alteration of homeobox gene expression by N-ras transformation of PA-1 human teratocarcinoma cells.

1991 ◽  
Vol 11 (7) ◽  
pp. 3573-3583 ◽  
Author(s):  
R Buettner ◽  
S O Yim ◽  
Y S Hong ◽  
E Boncinelli ◽  
M A Tainsky
Keyword(s):  
Cell Differentiation ◽  
Growth Regulation ◽  
Homeobox Genes ◽  
Constitutive Expression ◽  
Homeobox Gene ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
Transformed Cells ◽  
Teratocarcinoma Cell ◽  
Cell Clones

We used a series of cell clones from a human teratocarcinoma cell line, PA-1, to study the effect of transformation by an activated N-ras oncogene on the expression of genes involved in retinoic acid (RA)-induced differentiation and growth regulation. Recently, it has been shown that expression of human HOX 2 genes is sequentially activated by RA beginning from Hox 2.9 at the 3' end of the HOX 2 cluster (A. Simeone, D. Acampora, L. Arcioni, P. W. Andrews, E. Boncinelli, and F. Mavilio, Nature [London] 346:763-766, 1990). We now report that six different genes of the cluster HOX 1 are sequentially induced by RA in a similar temporal pattern, beginning with genes at the 3' end of the cluster. However, in N-ras-transformed cell clones, RA-induced expression of these homeobox genes is delayed. Hox 1.4 and Hox 1.3, genes abundantly induced in nontransformed clones after 3 days of RA treatment, are expressed in N-ras-transformed cells only after 10 days of RA treatment. At this time, the cells' growth is arrested at very high density, and no differentiated morphologic characteristics are observed. Constitutive expression of a transfected Hox 1.4 gene under the control of a simian virus 40 promotor leads to differentiated cell morphology similar to that of the RA-induced phenotype and restores the growth-inhibitory effects of RA in N-ras-transformed cells. These observations provide evidence that enhanced proliferation in N-ras-transformed cells compromises teratocarcinoma cell differentiation by a mechanism that transiently suppresses homeobox gene induction and implies a central role for homeobox genes in RA-induced cell differentiation. We conclude that stimulation of a putative growth factor signal pathway, associated with ras-induced proliferation, transiently suppresses the induction of transcription factors functionally involved in cell growth and differentiation.

Cell surface alteration in Epstein-Barr virus-transformed cells from patients with extreme insulin resistance

Diabetes ◽  
1990 ◽  
Vol 39 (8) ◽  
pp. 924-927 ◽  
Author(s):  
D. L. Gorden ◽  
A. Robert ◽  
V. Y. Moncada ◽  
S. I. Taylor ◽  
J. Muhlhauser ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Cell Surface ◽  
Epstein Barr Virus ◽  
Transformed Cells ◽  
Barr Virus ◽  
Surface Alteration ◽  
Extreme Insulin Resistance ◽  
Epstein Barr
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