Myeloproliferative virus, a cloned murine sarcoma virus with spleen focus-forming properties in adult mice

Ostertag, Wolfram; Vehmeyer, K.; Fagg, Barbara; Pragnell, Ian B.; Paetz, W; bousse, M C Le; Smadja-Joffe, Florence; Klein, Bernard; Jasmin, C; Eisen, Harvey

doi:10.1128/jvi.33.2.573-582.1980

Cited by 94 publications

(57 citation statements)

References 22 publications

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“…Plasmids and probes. The retroviral vectors Neor MPSV and Neor mos-, derivatives of MPSV (21,28), were previously described in detail (27) and are represented schematically in Fig. 1.…”

Section: Methodsmentioning

confidence: 99%

Murine gamma interferon inhibits v-mos-induced fibroblast transformation via down regulation of retroviral gene expression

Seliger¹,

Kruppa²,

Pfizenmaier³

1987

J Virol

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Expression of the retroviral vector Neor myeloproliferative sarcoma virus (MPSV), which contains the v-mos oncogene and the neomycin resistance gene, leads to neoplastic transformation of mouse fibroblasts. Murine recombinant gamma interferon (IFN-y) could revert the neoplastic properties of established Neor MPSVtransformed cell lines to an apparently untransformed phenotype. In the presence of IFN-y, the Neor MPSV transformants showed a greater than 97% reduction of cloning efficiency in soft agar, strongly reduced proliferative capacity, and morphological changes. The IFN-y-induced phenotypic reversion was preceded by a rapid and selective reduction of all retroviral RNA species, apparently due to IFN-y action on the long terminal repeat of Neor MPSV. The mRNA levels of cellular genes either remained unaffected (,I-actin) or were even enhanced (H-2) in IFN-y-treated Neor MPSV-transformed cells. Upon removal of IFN-y, retroviral gene expression was fully recovered and a gradual reappearance of the transformed phenotype of these cells within 3 weeks was noted. These data show that IFN-'y can cause a virtually complete, but reversible, inhibition of v-mos-induced neoplastic properties in transformed fibroblasts by selective down regulation of retroviral RNA levels.

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“…Plasmids and probes. The retroviral vectors Neor MPSV and Neor mos-, derivatives of MPSV (21,28), were previously described in detail (27) and are represented schematically in Fig. 1.…”

Section: Methodsmentioning

confidence: 99%

Murine gamma interferon inhibits v-mos-induced fibroblast transformation via down regulation of retroviral gene expression

Seliger¹,

Kruppa²,

Pfizenmaier³

1987

J Virol

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“…Tumor cells of the parental clone and the subclone were grown in Dulbecco's minimum essential medium (Biochrom, Berlin, FRG) containing 10% fetal calf serum (FCS), 2 % L-glutamine and antibiotics, and were harvested after 4-5 days. Clone 6-6#3+F was derived from transformation of rat fibroblasts (NRK) with a myeloproliferative virus (MPV) (Ostertag et at., 1980). The cell line was grown in RPMI-1640 medium (Biochrom), supplemented with 20 m~ HEPES, 4 m~ L-glutamine, 200 pg/ml penicillin-streptomycin and 10% FCS (Gibco, Karlsruhe, FRG).…”

Section: Cell Lines Culture Conditions and Tumorsmentioning

confidence: 99%

Differential expression of endogenous sugar‐binding proteins (lectins) in murine tumor model systems with metastatic capacity

Gabius

Bandlow

Schirrmacher

et al. 1987

Intl Journal of Cancer

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In order to investigate possible differences in sugar binding activities of strongly versus weakly metastatic tumors, sugar-binding molecules (endogenous lectins) of murine tumor cells differing in metastatic capacity were analyzed by affinity chromatography on supports with immobilized sugars or glycoproteins and compared. After elution with specific sugar in the absence of Ca2+-ions, the proteins were separated by sodium dodecyl sulfate-polyacrylamide slab gel electrophoresis. In comparison to a weakly metastatic subline (Eb) spontaneous strongly metastatic variants (ESb) of a murine lymphoma contained additional sugar receptors for N-acetylglucosamine (Mr 30 kDa) and maltose (Mr 64 kDa, 62 kDa, 54 kDa and 32 kDa), and lacked one sugar receptor for myoinositol (Mr 85 kDa), N-acetylglucosamine (Mr 23 kDa) and maltose (Mr 22 kDa), respectively. The strongly metastatic variant ESb expressed the common beta-galactoside-specific lectin to a higher extent and receptors for myo-inositol, melibiose and mannan to a lower extent. In another model system derived from the murine mastocytoma cell line P 815 X 2A, biochemical analysis of the liver-metastasizing variant P 815 X 2B revealed additional characteristic N-acetylgalactosamine- and maltose-specific binding proteins. This variant had reduced amounts of receptors for beta-galactosides and fucose in comparison to the parental clone. In a third tumor system a similar qualitative difference was disclosed: a metastatic variant derived from spleen metastases displayed a sugar receptor profile with 5 additional beta-galactoside-binding proteins when compared to its parental clone 6-6#3 + F, which is a virally transformed fibroblast line. The results show that metastatic variants of 3 murine tumor models consisting of lymphomas, mastocytomas and sarcomas are characterized by qualitative and quantitative alterations in the profiles of sugar-binding proteins.

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“…A related virus, the myeloproliferative sarcoma virus (MPSV) (25), arose as a spontaneous mutant of the Moloney murine sarcoma virus (MSV), which caused myeloproliferative disorders instead of sarcomas. Several groups have demonstrated that MPSV has greater transcriptional activity than Mo-MuLV in EC cells (20,21,50) and in hematopoietic cells (4,39,46). The LTR of MPSV has several base-pair changes compared to the LTR sequences of Mo-MuLV and MSV, with one single-base-pair alteration in the enhancer of MPSV creating a consensus binding site for the Sp1 transcription factor; this new Sp1 site was shown to be responsible for the altered pathogenic pattern of MPSV and increased transcriptional activity in EC cells (41).…”

mentioning

confidence: 99%

Increased probability of expression from modified retroviral vectors in embryonal stem cells and embryonal carcinoma cells

Robbins

Skelton

et al. 1997

J Virol

119

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Gene expression from the Moloney murine leukemia retrovirus (Mo-MuLV) is highly restricted in embryonic carcinoma (EC) and embryonic stem (ES) cells. We compared levels of expression in PA317 fibroblasts, F9 (EC) cells, and CCE (ES) cells by Mo-MuLV-based vectors and vectors based on our previously reported MND backbone, which has alterations to address three viral elements implicated as repressors of expression byMo-MuLV: the enhancer, the primer binding site, and the negative-control region. Expression was evaluated with three reporter genes, the chloramphenicol acetyltransferase (CAT) gene, whose expression was measured by enzymatic assay and by Northern blotting; a truncated nerve growth factor receptor (tNGFR), whose expression was measured by fluorescence-activated cell sorting (FACS) as a cell surface protein; and the enhanced green fluorescent protein (EGFP), whose expression was measured intracellularly by flow cytometry. We found significantly higher levels of CAT activity (5-to 300-fold) and greater quantities of vector-specific transcripts in ES and EC cells transduced with the modified MND-CAT-SN vector than in those transduced with L-CAT-SN. Northern blot analysis indicated that long terminal repeat transcripts from MND-CAT-SN are >80 times more abundant than the L-CAT-SN transcripts. FACS analysis of tNGFR expression from a pair of vectors, L-tNGFR-SN and MND-tNGFR-SN, indicated that only 1.04% of the CCE cells containing the L-tNGFR-SN vector expressed the cell surface reporter, while the MND-tNGFR-SN vector drove expression in 99.54% of the CCE cells. Of the F9 cells containing the L-tNGFR-SN vector, 13.32% expressed tNGFR, while 99.89% of the F9 cells transduced with MND-tNGFR-SN showed expression. Essentially identical results were produced with an analogous pair of vectors encoding EGFP. In unselected pools of F9 cells 48 h posttransduction, the L-EGFP-SN vector drove expression in only 5% of the population while the MND-EGFP-SN vector drove expression in 88% of the cells. After more than 3 weeks in culture without selection, the proportion of cells showing expression from L-EGFP-SN decreased slightly to 3% while expression from the MND-EGFP-SN vector persisted in 80% of the cells. Interestingly, in the few ES and EC cells which did show expression fromthe L-tNGFR-SN or L-EGFP-SN vectors, the magnitude of reporter expression was similar to that from the MND-tNGFR-SN or MND-EGFP-SN vector in nearly all cells, suggesting that the MND vectors are far less susceptible to position-dependent variegation of expression than are the Mo-MuLV-based vectors. Therefore, the modified retroviral vector, MND, achieves higher net levels of expression due to a greater frequency of expression, which may be useful for the expression of exogenous genes in EC and ES cells.

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Myeloproliferative virus, a cloned murine sarcoma virus with spleen focus-forming properties in adult mice

Cited by 94 publications

References 22 publications

Murine gamma interferon inhibits v-mos-induced fibroblast transformation via down regulation of retroviral gene expression

Murine gamma interferon inhibits v-mos-induced fibroblast transformation via down regulation of retroviral gene expression

Differential expression of endogenous sugar‐binding proteins (lectins) in murine tumor model systems with metastatic capacity

Increased probability of expression from modified retroviral vectors in embryonal stem cells and embryonal carcinoma cells

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