Clonal analysis of the change in growth phenotype during embryonal carcinoma cell differentiation

1982 ◽  
Vol 58 (1) ◽  
pp. 331-344
Author(s):  
M.J. Rayner ◽  
C.F. Graham
Keyword(s):  
Growth Rate ◽  
Retinoic Acid ◽  
Embryonal Carcinoma ◽  
Carcinoma Cells ◽  
Embryonal Carcinoma Cell ◽  
Clonal Level ◽  
Ec Cells ◽  
Growth Phenotype ◽  
Derivatives Of ◽  
Do So

Retinoic acid has been shown to induce the differentiation of mouse embryonal carcinoma cells. Previous workers have reported that bulk cultures of the differentiated derivatives have a slower growth rate and a reduced capacity to form tumours. We have analysed this change in growth rate for a sub-tetraploid EC cell line, PC13 clone 5 MA2, at a clonal level and have shown that the production of cells with a slower growth rate is not a result of cell selection. We have also demonstrated that the action of retinoic acid on growth rate is delayed for approximately 48 h and that the new growth phenotype, once attained, is stable. Finally we have confirmed at a clonal level that the differentiated derivatives of EC cells exposed to retinoic acid have a reduced capacity to form tumours. Clones of EC cells exposed to retinoic acid for longer than 96 h are unable to form tumours in a 30-day period, whilst 87% of their untreated counterparts are able to do so.

Effects of methylmercury on retinoic acid-induced neuroectodermal derivatives of embryonal carcinoma cells

1988 ◽  
Vol 4 (1) ◽  
pp. 61-80 ◽  
Author(s):  
Monique Cadrin ◽  
Geoffrey O. Wasteneys ◽  
Elizabeth M. V. Jones-Villeneuve ◽  
David L. Brown ◽  
Kenneth R. Reuhl
Keyword(s):  
Retinoic Acid ◽  
Embryonal Carcinoma ◽  
Carcinoma Cells ◽  
Embryonal Carcinoma Cells ◽  
Derivatives Of

Dickkopf-3 alters the morphological response to retinoic acid during neuronal differentiation of human embryonal carcinoma cells

2014 ◽  
Vol 74 (12) ◽  
pp. 1243-1254 ◽  
Author(s):  
Rocío Jiménez Alfonso ◽  
Irantzu Gorroño-Etxebarria ◽  
Miriam Rabano ◽  
Maria dM. Vivanco ◽  
Robert Kypta
Keyword(s):  
Retinoic Acid ◽  
Neuronal Differentiation ◽  
Embryonal Carcinoma ◽  
Carcinoma Cells ◽  
Embryonal Carcinoma Cells ◽  
Morphological Response

Expression of the Brachyury gene during mesoderm development in differentiating embryonal carcinoma cell cultures

Development ◽  
1994 ◽  
Vol 120 (1) ◽  
pp. 115-122 ◽  
Author(s):  
G. Vidricaire ◽  
K. Jardine ◽  
M.W. McBurney
Keyword(s):  
Bone Morphogenetic Proteins ◽  
Embryonal Carcinoma ◽  
Carcinoma Cell ◽  
Cell Aggregation ◽  
Cell Types ◽  
Carcinoma Cells ◽  
Embryonal Carcinoma Cell ◽  
P19 Cells ◽  
Mesoderm Development ◽  
P19 Embryonal Carcinoma Cells

When aggregated and treated with dimethyl sulfoxide (DMSO), P19 embryonal carcinoma cells differentiate into cell types normally derived from the mesoderm and endoderm including epithelium and cardiac and skeletal muscle. The Brachyury gene is expressed transiently in these differentiating cultures several days before the appearance of markers of the differentiated cell types. The expression of Brachyury is not affected by DMSO but is induced by cell aggregation, which requires extracellular calcium. Expression of Brachyury is also induced by various members of the TGF beta family such as activin and bone morphogenetic proteins. D3 is a mutant clone of P19 cells selected for its failure to differentiate when aggregated in DMSO. Aggregated D3 cells express Brachyury mRNA suggesting that the mutation(s) responsible for the phenotype of D3 cells is downstream of the chain of events initiated by Brachyury expression.

scholarly journals Modulation of dexamethasone receptor expression in embryonal carcinoma cells and their differentiated derivatives

1982 ◽  
Vol 208 (1) ◽  
pp. 235-238 ◽  
Author(s):  
Clare M. Isacke ◽  
John K. Heath
Keyword(s):  
Glucocorticoid Receptors ◽  
Embryonal Carcinoma ◽  
Binding Capacity ◽  
Culture Conditions ◽  
Carcinoma Cells ◽  
Receptor Expression ◽  
Embryonal Carcinoma Cell ◽  
Embryonal Carcinoma Cells ◽  
Epidermal Growth ◽  
Cell Culture Conditions

The dexamethasone binding capacity of embryonal carcinoma cells and their differentiated derivatives was investigated. Manipulation of the embryonal carcinoma cell-culture conditions resulted in an unstable reversible expression of the glucocorticoid receptors. Stable expression of the receptors is observed when these cells are induced to differentiate. Cells grown under identical conditions were assayed for their ability to bind epidermal growth factor.

scholarly journals Retinoic acid induces embryonal carcinoma cells to differentiate into neurons and glial cells.

1982 ◽  
Vol 94 (2) ◽  
pp. 253-262 ◽  
Author(s):  
E M Jones-Villeneuve ◽  
M W McBurney ◽  
K A Rogers ◽  
V I Kalnins
Keyword(s):  
Retinoic Acid ◽  
Glial Cells ◽  
Embryonal Carcinoma ◽  
Acetylcholinesterase Activity ◽  
Cell Types ◽  
Carcinoma Cells ◽  
Embryonal Carcinoma Cells ◽  
Neurofilament Protein ◽  
Acid Toxicity ◽  
Precocious Development

Murine embryonal carcinoma cells can differentiate into a varied spectrum of cell types. We observed the abundant and precocious development of neuronlike cells when embryonal carcinoma cells of various pluripotent lines were aggregated and cultured in the presence of nontoxic concentrations of retinoic acid. Neuronlike cells were also formed in retinoic acid-treated cultures of the embryonal carcinoma line, P19, which does not differentiate into neurons in the absence of the drug. The neuronal nature of these cells was confirmed by their staining with antiserum directed against neurofilament protein in indirect immunofluorescence experiments. Retinoic acid-treated cultures also contained elevated acetylcholinesterase activity. Glial cells, identified by immunofluorescence analysis of their intermediate filaments, and a population of fibroblastlike cells were also present in retinoic acid-treated cultures of P19 cells. We did not observe embryonal carcinoma, muscle, or epithelial cells in these cultures. Neurons and glial cells appeared in cultures exposed to retinoic acid for as little as 48 h. We found no evidence for retinoic acid toxicity, suggesting that the effect of the drug was to induce the development of neurons and glia rather than to select against cells differentiating along other developmental pathways.

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