scholarly journals Imsnc761 and DDX6 synergistically suppress cell proliferation and promote apoptosis via p53 in testicular embryonal carcinoma cells

2018 ◽  
Vol 38 (4) ◽  
Author(s):  
Zhengzheng Duan ◽  
Ping Ping ◽  
Guishuan Wang ◽  
Xiansheng Zhang ◽  
Fei Sun
Keyword(s):  
Embryonal Carcinoma ◽  
Carcinoma Cells ◽  
Specific Gene ◽  
Embryonal Carcinoma Cell ◽  
Label Free ◽  
Kegg Pathways ◽  
Dead Box ◽  
Eukaryotic Organisms ◽  
Quantitation Method ◽  
Normal Controls

Intermediate-sized non-coding RNAs (imsncRNAs) have been shown to play important regulatory roles in the development of several eukaryotic organisms. In the present research, we selected imsncRNA 761 (imsnc761) as a research target. Expression analyses in a previous study showed that imsnc761 was down-regulated in maturation-arrested testis tissues as compared with the level in normal controls. In the present study, we found that imsnc761 could interact with DEAD-box helicase 6 (DDX6) to induce NTERA-2 (NT2 (testicular embryonal carcinoma cell)) cell apoptosis and proliferation inhibition via the p53 pathway. This interaction between imsnc761 and DDX6 also inhibited mitochondrial function and specific gene transcription and translation. To facilitate further research, we used label-free quantitation method to analyze the associated differences in Kyoto Encyclopaedia of Genes and Genomes (KEGG) pathways and biological processes. This confirmed the changes in several specific pathways, which matched our molecular experimental results.

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 Expression of simian virus 40 large T antigen in embryonal carcinoma cell hybrids.

1984 ◽  
Vol 4 (8) ◽  
pp. 1657-1660 ◽  
Author(s):  
A Tunnacliffe ◽  
L V Crawford ◽  
P Goodfellow
Keyword(s):  
Embryonal Carcinoma ◽  
Carcinoma Cell ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
T Antigen ◽  
Carcinoma Cells ◽  
Embryonal Carcinoma Cell ◽  
Embryonal Carcinoma Cells ◽  
Large T Antigen ◽  
Early Region

Previous work has shown that murine embryonal carcinoma cells are refractory to infection with various viruses, including simian virus 40. Thus, large T and small t antigens, the products of the simian virus 40 early region, are not produced when the virus infects embryonal carcinoma cells, in contrast to other cell types. We show, by qualitative and quantitative analyses, that embryonal carcinoma cell hybrids, containing a simian virus 40 early region integrated into human DNA, are capable of producing viral large T antigen.

scholarly journals A novel keratan sulphate proteoglycan from a human embryonal carcinoma cell line

1992 ◽  
Vol 286 (3) ◽  
pp. 959-966 ◽  
Author(s):  
S Cooper ◽  
M F Pera ◽  
W Bennett ◽  
J T Finch
Keyword(s):  
Embryonal Carcinoma ◽  
Broad Band ◽  
Gel Filtration ◽  
Exchange Chromatography ◽  
Carcinoma Cells ◽  
Embryonal Carcinoma Cell ◽  
Embryonal Carcinoma Cells ◽  
Keratan Sulphate ◽  
Major Band ◽  
Sulphate Proteoglycan

We describe here the purification and partial characterization of a 200 kDa keratan sulphate proteoglycan found in the pericellular matrix of human embryonal carcinoma cells. Previously we have shown that this molecule is recognized by a monoclonal antibody (GCTM-2). The antigen was isolated using ion-exchange chromatography and gel filtration, purification being monitored by e.l.i.s.a. using GCTM-2. Metabolic labelling of GCT 27 C-4 embryonal carcinoma cells with sodium [35S]sulphate resulted in the incorporation of [35S]sulphate into the purified molecule. Throughout the purification procedure, the peaks of 35S radioactivity were coincident with the peaks of immunoreactivity, and this label was released both by digestion with keratanase and chondroitinase, confirming the proteoglycan nature of the antigen. The intact molecule ran as a single broad band of 200 kDa, which has been identified by silver staining and immunoblotting following gel electrophoresis. Amino acid analysis of the purified antigen indicated a high content of serine, glycine and aspartic acid/asparagine residues. Visualization by rotary-shadowing electron microscopy suggests that the purified material forms large aggregates, even under denaturing conditions. Deglycosylation of this preparation with trifluoromethanesulphonic acid yielded a major band of 55 kDa and a minor band of 48 kDa. The biochemical nature of the molecule described here, along with tissue distribution studies using GCTM-2, indicates that the antigen is not related to previously described keratan sulphate proteoglycans.

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.

scholarly journals Ribonucleoprotein particles with LINE-1 RNA in mouse embryonal carcinoma cells.

1991 ◽  
Vol 11 (9) ◽  
pp. 4804-4807 ◽  
Author(s):  
S L Martin
Keyword(s):  
Embryonal Carcinoma ◽  
Mouse Genome ◽  
Carcinoma Cell ◽  
Carcinoma Cells ◽  
Embryonal Carcinoma Cell ◽  
Embryonal Carcinoma Cells ◽  
Ribonucleoprotein Particle ◽  
Repeat Family ◽  
Embryonal Carcinoma Cell Line ◽  
Mammalian Genomes

The LINE-1 repeat family is interspersed throughout mammalian genomes and is thought to be the result of duplicative transposition of LINE-1 sequences via an RNA intermediate. This report describes a ribonucleoprotein particle with LINE-1 RNA in the mouse embryonal carcinoma cell line F9. This ribonucleoprotein particle is a potential intermediate in the transposition of LINE-1 in the mouse genome.

Ribonucleoprotein particles with LINE-1 RNA in mouse embryonal carcinoma cells

1991 ◽  
Vol 11 (9) ◽  
pp. 4804-4807
Author(s):  
S L Martin
Keyword(s):  
Embryonal Carcinoma ◽  
Mouse Genome ◽  
Carcinoma Cell ◽  
Carcinoma Cells ◽  
Embryonal Carcinoma Cell ◽  
Embryonal Carcinoma Cells ◽  
Ribonucleoprotein Particle ◽  
Repeat Family ◽  
Embryonal Carcinoma Cell Line ◽  
Mammalian Genomes

The LINE-1 repeat family is interspersed throughout mammalian genomes and is thought to be the result of duplicative transposition of LINE-1 sequences via an RNA intermediate. This report describes a ribonucleoprotein particle with LINE-1 RNA in the mouse embryonal carcinoma cell line F9. This ribonucleoprotein particle is a potential intermediate in the transposition of LINE-1 in the mouse genome.

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