Minute virus of mice inhibits cell transformation by simian virus 40

Nature ◽  
1982 ◽  
Vol 300 (5892) ◽  
pp. 537-539 ◽  
Author(s):  
S. Mousset ◽  
J. Rommelaere
Keyword(s):  
Cell Transformation ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
Minute Virus Of Mice ◽  
Minute Virus

scholarly journals Simian virus 40 and cancer

2011 ◽  
pp. 131-140
Author(s):  
Sandra Eliasz ◽  
Michele Carbone ◽  
Maurizio Bocchetta
Keyword(s):  
Molecular Biology ◽  
Human Population ◽  
Animal Studies ◽  
Cell Transformation ◽  
Human Cancer ◽  
Mesothelial Cell ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
Oncogenic Virus ◽  
Experimental Approaches

Since its discovery in 1960 as a contaminant of poliovaccines, Simian Virus 40 (SV40) has been the object of extensive studies to assess whether this oncogenic virus plays a role in human carcinogenesis. Over the last two decades, this question has met with broad scepticism. However, there is increasing evidence linking SV40 to specific types of human cancer, especially malignant mesothelioma. Recently, two laboratories using different experimental approaches independently confirmed that SV40 acts synergistically with environmental fibers to promote mesothelial cell transformation and mesothelioma. Most of the scepticism concerning SV40 and cancer was due to the lack of clear epidemiologic data. However, it is still not clear how SV40 circulates in the human population, making the identification of SV40-exposed versus non-exposed cohorts problematic. Consequently, the most helpful insights into SV40-mediated carcinogenesis have come from molecular pathology, cell and molecular biology, and from animal studies.

scholarly journals Enumeration of the Simian Virus 40 Early Region Elements Necessary for Human Cell Transformation

2002 ◽  
Vol 22 (7) ◽  
pp. 2111-2123 ◽  
Author(s):  
William C. Hahn ◽  
Scott K. Dessain ◽  
Mary W. Brooks ◽  
Jessie E. King ◽  
Brian Elenbaas ◽  
...  
Keyword(s):  
Cell Transformation ◽  
Human Tumor ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
Experimental Models ◽  
T Antigen ◽  
Human Cells ◽  
Sv40 Large T Antigen ◽  
Early Region ◽  
Intracellular Pathways

ABSTRACT While it is clear that cancer arises from the accumulation of genetic mutations that endow the malignant cell with the properties of uncontrolled growth and proliferation, the precise combinations of mutations that program human tumor cell growth remain unknown. The study of the transforming proteins derived from DNA tumor viruses in experimental models of transformation has provided fundamental insights into the process of cell transformation. We recently reported that coexpression of the simian virus 40 (SV40) early region (ER), the gene encoding the telomerase catalytic subunit (hTERT), and an oncogenic allele of the H-ras gene in normal human fibroblast, kidney epithelial, and mammary epithelial cells converted these cells to a tumorigenic state. Here we show that the SV40 ER contributes to tumorigenic transformation in the presence of hTERT and oncogenic H-ras by perturbing three intracellular pathways through the actions of the SV40 large T antigen (LT) and the SV40 small t antigen (ST). LT simultaneously disables the retinoblastoma (pRB) and p53 tumor suppressor pathways; however, complete transformation of human cells requires the additional perturbation of protein phosphatase 2A by ST. Expression of ST in this setting stimulates cell proliferation, permits anchorage-independent growth, and confers increased resistance to nutrient deprivation. Taken together, these observations define the elements of the SV40 ER required for the transformation of human cells and begin to delineate a set of intracellular pathways whose disruption, in aggregate, appears to be necessary to generate tumorigenic human cells.

scholarly journals Elevated recombination in immortal human cells is mediated by HsRAD51 recombinase.

1997 ◽  
Vol 17 (12) ◽  
pp. 7151-7158 ◽  
Author(s):  
S J Xia ◽  
M A Shammas ◽  
R J Shmookler Reis
Keyword(s):  
Cell Lines ◽  
Cell Transformation ◽  
Human Fibroblasts ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
T Antigen ◽  
Cell Strains ◽  
Immortal Cells ◽  
Diploid Cells ◽  
Untransformed Cell

Normal diploid cells have a limited replicative potential in culture, with progressively increasing interdivision time. Rarely, cell lines arise which can divide indefinitely; like tumor cells, such "immortal" lines display frequent chromosomal aberrations which may reflect high rates of recombination. Recombination frequencies within a plasmid substrate were 3.5-fold higher in nine immortal human cell lines than in six untransformed cell strains. Expression of HsRAD51, a human homolog of the yeast RAD51 and Escherichia coli recA recombinase genes, was 4.5-fold higher in immortal cell lines than in mortal cells. Stable transformation of human fibroblasts with simian virus 40 large T antigen prior to cell immortalization increased both chromosomal recombination and the level of HsRAD51 transcripts by two- to fivefold. T-antigen induction of recombination was efficiently blocked by introduction of HsRAD51 antisense (but not control) oligonucleotides spanning the initiation codon, implying that HsRAD51 expression mediates augmented recombination. Since p53 binds and inactivates HsRAD51, T-antigen-p53 association may block such inactivation and liberate HsRAD51. Upregulation of HsRAD51 transcripts in T-antigen-transformed and other immortal cells suggests that recombinase activation can also occur at the RNA level and may facilitate cell transformation to immortality.

Genetics of Cell Transformation by Simian Virus 40

1974 ◽  
Vol 39 (0) ◽  
pp. 335-343 ◽  
Author(s):  
C. M. Croce ◽  
K. Huebner ◽  
A. J. Girardi ◽  
H. Koprowski
Keyword(s):  
Cell Transformation ◽  
Simian Virus 40 ◽  
Simian Virus

N-terminal amino acid sequences of the polyoma middle-size T antigen are important for protein kinase activity and cell transformation

1984 ◽  
Vol 4 (5) ◽  
pp. 817-821
Author(s):  
D Templeton ◽  
W Eckhart
Keyword(s):  
Protein Kinase ◽  
Kinase Activity ◽  
Cell Transformation ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
T Antigen ◽  
Amino Acid Sequences ◽  
Protein Kinase Activity ◽  
Terminal Amino Acid ◽  
Terminal Amino

We constructed deletion mutations which removed N-terminal coding sequences of various lengths from a cloned polyoma middle-size T antigen (MT antigen) gene. We introduced the MT antigen genes into a simian virus 40 expression vector so that they were expressed at high levels under the control of the simian virus 40 late promoter in COS-1 cells. The deletion mutant genes synthesized truncated MT antigens whose size was consistent with the deletion of either 70 or 106 amino acids from N termini, owing to initiation of translation at internal methionine codons in the MT antigen-coding region. The truncated MT antigens were found in cell membrane fractions but failed to show MT antigen-associated protein kinase activity. The cloned deletion mutant DNAs failed to transform rat F2408 or mouse NIH 3T3 cells. Therefore, N-terminal amino acid sequences of the polyoma MT antigen, as well as C-terminal sequences, are important for protein kinase activity and cell transformation.

scholarly journals Enumeration of the Simian Virus 40 Early Region Elements Necessary for Human Cell Transformation

2002 ◽  
Vol 22 (10) ◽  
pp. 3562-3562 ◽  
Author(s):  
William C. Hahn ◽  
Scott K. Dessain ◽  
Mary W. Brooks ◽  
Jessie E. King ◽  
Brian Elenbaas ◽  
...  
Keyword(s):  
Human Cell ◽  
Cell Transformation ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
Early Region
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