Limitations to the expression of parvoviral nonstructural proteins may determine the extent of sensitization of EJ-ras-transformed rat cells to minute virus of mice

Hille, B van; Duponchel, N.; Salomé, Nathalie; Spruyt, Nathalie; Cotmore, S F; Tattersall, Peter; Cornelis, Jan J.; Rommelaere, Jean

doi:10.1016/0042-6822(89)90514-x

Cited by 45 publications

(54 citation statements)

References 22 publications

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“…3) paralleled that of virus cytotoxicity ( Table 1), suggesting that the latter may reflect, at least in part, the capacity of cells for expressing the MVMp NS genes. A similar correlation has been reported recently for a series of related ras-transformed rat fibroblasts (van Hille et al, 1989). Together, these data indicate that various oncogenes or combinations thereof are able to interfere in a distinct and positive way with the control of NS protein production in parvovirus-infected cells.…”

Section: Oncogene-induced Modulation Of Mvmp Replicationsupporting

confidence: 88%

“…The transformed cell lines FRLT1, FRMC14 and FREJ4 have been described previously by Rassoulzadegan et al (1982), Salom6 et al (t990) and van Hille et al (1989), respectively. FR4 derivatives transformed by PyMT (FRMT) or both PyMT and PyLT (FRMLT) were isolated as geneticin (0-5 mg/ml)-resistant foci of morphologically altered cells, after cotransfection with plasmid pSV2neo (Southern & Berg, 1982) and pPyMT1 (Treisman et al, 1981) or pPyMLT97 (Gelinas et al, 1989).…”

Section: Methodsmentioning

confidence: 99%

“…This oncotropism is consistent with the fact that a number of neoplastic or transformed cells cultivated in vitro are permissive to the lytic parvovirus life cycle, whereas 0001-0911 © 1992 SGM normal cells generally resist virus attack. This sensitization of transformed cells correlates with a stimulation of parvoviral gene expression, suggesting that some viral proteins may be cytotoxic (Rhode, 1987;Osawa et al, 1988;Cornelis et al, 1988b;van Hille et al, 1989;Brandenburger et al, 1990). It has been demonstrated recently that the intracellular accumulation of MVMencoded regulatory non-structural (NS) proteins is toxic for neoplastic human cells (Caillet-Fauquet et al, 1990).…”

Section: Introductionmentioning

confidence: 99%

“…It has been shown that tumour viruses, cellular or viral oncogenes, and chemical or physical carcinogens may sensitize normally resistant cells to parvovirus-induced killing (Mousset & Rommelaere, 1982;Mousset et al, 1986;Cornelis et al, 1988a;van Hille et aL, 1989;Salem6 et al, 1990;Guetta et al, 1990). However, it is unclear whether cell sensitization to parvoviruses correlates with the expression of a specific facet(s) of the transformed phenotype.…”

Section: Introductionmentioning

confidence: 99%

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Cooperation of oncogenes in cell transformation and sensitization to killing by the parvovirus minute virus of mice

Legrand

Mousset

Salomé

et al. 1992

Journal of General Virology

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Section: Oncogene-induced Modulation Of Mvmp Replicationsupporting

confidence: 88%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Cooperation of oncogenes in cell transformation and sensitization to killing by the parvovirus minute virus of mice

Legrand

Mousset

Salomé

et al. 1992

Journal of General Virology

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“…3 Cell killing appears to be due largely to the cytotoxicity of the viral nonstructural protein, NS1, which shows both enhanced levels of expression in transformed cells and preferential toxicity. 4,5 NS1 has multiple functions, including site-specific endonuclease activity, essential for replication of viral DNA, and transcriptional activation of the viral promoters. 1,6 Several members of the rodent parvovirus group can efficiently infect human transformed cell lines.…”

Section: Introductionmentioning

confidence: 99%

Control of parvovirus DNA replication by a tetracycline-regulated repressor

Maxwell

1999

Gene Ther

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Autonomous parvoviruses are small, single strand DNA construct unexpectedly showed constitutive expression in viruses which preferentially replicate in transformed and transiently transfected cells, as indicated by efficient excitumor cells, causing cell death by expression of the cytosion and amplification of viral replicative form (RF) DNA. toxic nonstructural protein, NS1. Several parvoviruses of This was apparently due to self-stimulatory transcriptional the rodent group, including LuIII, efficiently infect human transactivation by NS1. This problem was overcome by transformed cell lines. The potential for systemic use of cotransfection with a plasmid expressing a chimera of the these viruses in targeting metastases might be enhanced repressor of the tetracycline operon with a KRAB transif NS1 expression and viral replication could be controlled repression domain. These conditions allowed efficient conby an innocuous drug such as tetracycline. We therefore trol of transcription and RF amplification by the tetracycline substituted prokaryotic tetracycline operator sequences for derivative, doxycycline. These observations form a basis part of P4 of LuIII, the promoter responsible for transcripfor developing a therapeutic agent based on a drugtion of the mRNAs for nonstructural proteins. The resulting controlled parvovirus.

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Programmed killing of human cells by means of an inducible clone of parvoviral genes encoding non-structural proteins.

et al. 1990

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Although its dependence on the target cell type is well established, the cytopathogenicity of parvoviruses has remained elusive to date as far as its mechanism is concerned. However, indirect evidence suggested that parvoviral non‐structural (NS) proteins may be the cytotoxic effectors. In order to test this hypothesis, a molecular clone of parvovirus MVMp was modified, by replacing the P4 promoter of the NS transcription unit by the glucocorticoid‐inducible promoter of the mouse mammary tumour virus. Clones of neoplastic human cells that had incorporated this construct and that were induced to produce NS proteins by dexamethasone, showed a cytopathic effect and eventually died. Our data strongly suggest that the intracellular accumulation of parvoviral NS products jeopardizes the survival of the cells, which cannot be detected unless a threshold protein concentration is reached. Interestingly, a cell variant could be isolated which resisted dexamethasone‐induced killing, although it was fully inducible for the production of NS proteins. This variant was also unusually resistant to infection with MVMp virions, thus confirming the essential role played by the NS proteins in the parvoviral cytotoxicity and indicating that the cytocidal activity of the parvoviral NS products is modulated by cellular factors that may vary from one cell to another.

show abstract

Limitations to the expression of parvoviral nonstructural proteins may determine the extent of sensitization of EJ-ras-transformed rat cells to minute virus of mice

Cited by 45 publications

References 22 publications

Cooperation of oncogenes in cell transformation and sensitization to killing by the parvovirus minute virus of mice

Cooperation of oncogenes in cell transformation and sensitization to killing by the parvovirus minute virus of mice

Control of parvovirus DNA replication by a tetracycline-regulated repressor

Programmed killing of human cells by means of an inducible clone of parvoviral genes encoding non-structural proteins.

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