scholarly journals Structure of Normal and Polyoma Virus-Transformed Hamster Cell Cultures

1966 ◽  
Vol 1 (2) ◽  
pp. 169-173
Author(s):  
W. HOUSE ◽  
M. G. P. STOKER
Keyword(s):  
Cell Division ◽  
Cell Cultures ◽  
Polyoma Virus ◽  
Transformed Cells ◽  
Vertical Sections

Vertical sections of colonies and confluent sheets of normal and polyoma virus-transformed BHK21 cells, and of a spontaneous malignant variant of BHK21 cells, and also of freshly isolated hamster fibroblasts, were examined to determine the structural interrelationship of the cells in relation to their varying transplantability. All cells except the freshly isolated fibroblasts formed multilayers, but the virus-transformed cells were arranged in the form of a loose network, in which cell division took place. The untransformed BHK21 cells were very tightly packed and mitosis was rare. A spontaneous malignant variant which superficially resembled the normal BHK21 cells was shown by section to have features in common with virus-transformed cells.

scholarly journals Role of the Three Polyoma Virus Early Proteins in Tumorigenesis

1983 ◽  
Vol 3 (8) ◽  
pp. 1451-1459 ◽  
Author(s):  
Claude Asselin ◽  
Celine Gelinas ◽  
Marcel Bastin
Keyword(s):  
Cultured Cells ◽  
Virus Genome ◽  
T Antigen ◽  
Polyoma Virus ◽  
Transformed Cells ◽  
Newborn Rats ◽  
Wild Type ◽  
Complementary Function ◽  
Small T Antigen ◽  
Middle T Antigen

A modified polyoma virus genome which can encode the middle T protein but not the large or small T proteins transforms rat cells in culture with an efficiency about 20% that of the wild-type genome. Although middle T-transformed cells grow as tumors when transplanted into nude mice or syngeneic rats, the middle T gene alone is totally inactive when used in a more stringent and rigorous assay for tumorigenicity such as the injection of DNA into newborn rats. Thus, functions other than those expressed by middle T antigen are required for the elaboration of all the properties associated with tumorigenesis. To assess whether a complementary function could be exerted by the large or the small T antigen, we constructed plasmids containing two modified early regions which independently encoded middle T and one of the two other proteins. Both recombinants were tumorigenic in newborn rats. Cell lines derived by transfer of these plasmids under no special selective conditions did not acquire the property of growth in low-serum medium but exhibited the same tumorigenic properties as wild-type polyoma DNA-transformed cells. Furthermore, a recombinant which encoded the middle and small T antigens, but not the large T antigen, was tumorigenic in newborn rats. Although the small T antigen provides a complementary function for tumorigenicity, it cannot complement the middle T antigen for an efficient induction of transformation of cultured cells. This suggests that the complementary function exerted by the small T antigen is different from that of the N-terminal fragment of the large T protein.

scholarly journals The Respiration and Aerobic Glycolysis of Mouse Embryo Cell Cultures Infected with the SE Polyoma Virus.

1963 ◽  
Vol 17 supl. ◽  
pp. 55-58
Author(s):  
B. Skarzynski ◽  
M. Guminska ◽  
Z. Porwit-Bóbr ◽  
J. N. Baptist
Keyword(s):  
Cell Cultures ◽  
Mouse Embryo ◽  
Aerobic Glycolysis ◽  
Embryo Cell ◽  
Polyoma Virus ◽  
Mouse Embryo Cell

Properties of Polyoma virus-transformed cells II. Characteristics of the virus-specific RNA

1972 ◽  
Vol 18 (2) ◽  
pp. 247-254
Author(s):  
James B. Hudson
Keyword(s):  
Dna Hybridization ◽  
Infectious Virus ◽  
Specific Radioactivity ◽  
Polyoma Virus ◽  
Transformed Cells ◽  
Viral Genomes ◽  
High Specific Radioactivity ◽  
Mouse Cells ◽  
Covalently Linked ◽  
Competition Hybridization

The Polyoma virus-specific RNA (PyRNA) synthesized in a line of Polyoma-transformed hamster cells, was analyzed and compared with the viral-specific RNA synthesized "late" in productively infected mouse cells. The PyRNA from the transformed cells sedimented heterogeneously on sucrose gradients, including appreciable amounts of PyRNA in the > 40-S region. The overall sedimentation profile resembled that of "late" PyRNA synthesized in mouse cells. Competition hybridization experiments, however, revealed that the bulk of the PyRNA sequences in the transformed cells were different from "late" PyRNA sequences. The use of DNA–DNA hybridization experiments (with Polyoma DNA of high specific radioactivity) enabled an estimate to be made of the average number of viral genomes per transformed cell. No more than two, and possibly less than one, complete genomes were found. These studies support the hypothesis that this line of Polyoma transformed cells contains an incomplete genome, possibly only comprising "early" genes (hence the inability to rescue infectious virus), and that the viral RNA transcribed is covalently linked to host cell RNA moieties.

scholarly journals Lunasin: A Novel Cancer Preventive Seed Peptide that Modifies Chromatin

2008 ◽  
Vol 91 (4) ◽  
pp. 932-935 ◽  
Author(s):  
Ben O de Lumen
Keyword(s):  
Growth Rate ◽  
Cell Death ◽  
Cell Division ◽  
Skin Cancer ◽  
Mammalian Cells ◽  
Constitutive Expression ◽  
Epigenetic Mechanism ◽  
Transformed Cells ◽  
Chemical Carcinogens ◽  
Core Histones

Abstract Lunasin is a novel cancer preventive peptide whose efficacy against chemical carcinogens and oncogenes has been demonstrated in mammalian cells and a skin cancer mouse model. In contrast, constitutive expression of the lunasin gene in mammalian cells leads to arrest of cell division and cell death. Isolated and characterized in soy, lunasin peptide is also documented in barley and wheat and is predicted to be present in many more seeds because of its possible role in seed development. Initial studies show that lunasin is bioavailable in mice when orally ingested. Lunasin internalizes into mammalian cells within minutes of exogenous application, and localizes in the nucleus after 18 h. It inhibits acetylation of core histones in mammalian cells but does not affect the growth rate of normal and established cancer cell lines. An epigenetic mechanism of action is proposed whereby lunasin selectively kills cells being transformed or newly transformed cells by binding to deacetylated core histones exposed by the transformation event, disrupting the dynamics of histone acetylationdeacetylation.

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