Transformation of mammalian cells by avian myelocytomatosis virus and avian erythroblastosis virus

Quade, Kristina

doi:10.1016/0042-6822(79)90569-5

Cited by 166 publications

(72 citation statements)

References 14 publications

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“…Plasmid pLPONL contains a 732-bp HindIIIEcoRV fragment derived from the 5' nontranslated region of poliovirus type 2 (Lansing) (10) Cell Lines and Virus Production. The 293GP, PA317, and rat 208F cells have been described (7,12,13 (14). All cell lines in this study were maintained in high-glucose Dulbecco's modified essential medium (DMEM)/10o fetal calf serum.…”

Section: Methodsmentioning

confidence: 99%

A general method for the generation of high-titer, pantropic retroviral vectors: highly efficient infection of primary hepatocytes.

Yee

Miyanohara

LaPorte

et al. 1994

Proc. Natl. Acad. Sci. U.S.A.

467

328

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Section: Methodsmentioning

confidence: 99%

A general method for the generation of high-titer, pantropic retroviral vectors: highly efficient infection of primary hepatocytes.

Yee

Miyanohara

LaPorte

et al. 1994

Proc. Natl. Acad. Sci. U.S.A.

467

328

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“…We tested whether the JSRV Env protein could transform 208F rat embryo fibroblasts (15), a cell line with a very flat morphology that provides a good assay for oncogenic transformation (25). We used the pSX2.Jenv plasmid that we used to generate the PJ14 JSRV-pseudotype packaging cells (4) for the test.…”

Section: Hyal2 Has Low If Any Hyaluronidasementioning

confidence: 99%

“…Oncogenic Transformation Assay. 208F rat embryo fibroblasts (15) were seeded at 5 ϫ 10 5 per 6-cm dish in DMEM plus 10% FBS on day 1. On day 2, the cells were transfected with 10 g of plasmid DNA by using the CaPO 4 coprecipitation method as described (16).…”

Section: Analysis Of Hyal2 Expression In 293 Cells Transfected With Fmentioning

confidence: 99%

Candidate tumor suppressor HYAL2 is a glycosylphosphatidylinositol (GPI)-anchored cell-surface receptor for jaagsiekte sheep retrovirus, the envelope protein of which mediates oncogenic transformation

Sharath

Duh

Вигдорович

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

305

342

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Jaagsiekte sheep retrovirus (JSRV) can induce rapid, multifocal lung cancer, but JSRV is a simple retrovirus having no known oncogenes. Here we show that the envelope (env) gene of JSRV has the unusual property that it can induce transformation in rat fibroblasts, and thus is likely to be responsible for oncogenesis in animals. Retrovirus entry into cells is mediated by Env interaction with particular cell-surface receptors, and we have used phenotypic screening of radiation hybrid cell lines to identify the candidate lung cancer tumor suppressor HYAL2͞LUCA2 as the receptor for JSRV. HYAL2 was previously described as a lysosomal hyaluronidase, but we show that HYAL2 is actually a glycosylphosphatidylinositol (GPI)-anchored cell-surface protein. Furthermore, we could not detect hyaluronidase activity associated with or secreted by cells expressing HYAL2, whereas we could easily detect such activity from cells expressing the related serum hyaluronidase HYAL1. Although the function of HYAL2 is currently unknown, other GPI-anchored proteins are involved in signal transduction, and some mediate mitogenic responses, suggesting a potential role of HYAL2 in JSRV Env-mediated oncogenesis. Lung cancer induced by JSRV closely resembles human bronchiolo-alveolar carcinoma, a disease that is increasing in frequency and now accounts for Ϸ25% of all lung cancer. The finding that JSRV env is oncogenic and the identification of HYAL2 as the JSRV receptor provide tools for further investigation of the mechanism of JSRV oncogenesis and its relationship to human bronchiolo-alveolar carcinoma.J aagsiekte sheep retrovirus (JSRV) is the causative agent of a contagious lung cancer of sheep called ovine pulmonary carcinoma or sheep pulmonary adenomatosis (1). Tumors originate from type II secretory alveolar and nonciliated bronchiolar epithelial cells, and late stages of the disease are accompanied by the secretion of copious lung fluid containing the virus. Purified virus induces multifocal tumors in as little as 10 days (2), suggesting the role of a viral oncogene. However, JSRV is a simple retrovirus with typical gag, pol, and env genes and no known oncogenes. The viral structural (Gag) and enzymatic (Pol) proteins are unlikely to be responsible, because they interact primarily with viral components, but there is precedent for alteration of cellular functions by the envelope (Env) protein of retroviruses, which interacts with cellular components to mediate virus entry. For example, the deleted Env protein of the Friend spleen focus-forming virus causes erythroleukemia by binding to and activating the erythropoietin receptor (3). If the JSRV Env protein was indeed oncogenic, identification of the host cell receptor for JSRV would provide key insights into the oncogenic mechanism of this highly pathogenic retrovirus. Furthermore, the contagious nature of JSRV and its ability to survive exposure to proteases and surfactants present in lung fluid suggest that vectors based on JSRV might be useful for gene therapy targeted to the lung, pr...

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“…The parent cell line, the Fischer rat lung fibroblast 208F (Quade, 1979), was transfected with human c-myc linked to the Moloney virus LTR and a Hygromycin resistance marker (pHRMCGMI) using electroporation. Selection with Hygromycin B (HmB) was followed by picking single colonies as monoclonal cell lines (M7 and M8).…”

Section: Cell Linesmentioning

confidence: 99%

Susceptibility to apoptosis is differentially regulated by c-myc and mutated Ha-ras oncogenes and is associated with endonuclease availability

Arends

Mcgregor²,

Toft³

et al. 1993

Br J Cancer

115

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Summary Oncogenes and oncosuppressors can derugulate cell replication in tumours, and recently have been shown to influence the probability of apoptosis. The effects of human c-myc and mutated (T24) Ha-ras oncogenes on susceptibility to apoptosis were investigated by introducting them into immortalised rat fibroblasts. The resulting family of transfectants showed closely similar measures of proliferation, but widely divergent rates of apoptosis, differing by up to fifteen-fold, that correlated inversely with population expansion rates in vitro. T24-ras transfectants with moderate or high p2lras expression showed reduced apoptosis, and this was reversed by pharmacological inhibition of membrane localisation of p2l's by mevinolin. In contrast, c-myc stimulated apoptosis, and this was further enhanced by serum deprivation. Inducibility of effector proteins represents one possible mechanism of genetic control of the susceptibility to apoptosis, and its investigation showed that c-myc was associated with expression by viable cells of latent calcium/magnesium sensitive endonuclease activity characteristic of apoptosis. In contrast, endonuclease activity was not detected in viable cells of a T24-ras transfectant expressing high levels of p2lras. Thus, there appeared to be differential regulation of susceptibility to apoptosis, positively by c-myc and negatively by activated ras, and this was associated with availability of endonuclease activity. Genetic modulation of apoptosis in human neoplasms is likely to influence net growth rate, retention of cells acquiring new mutations and response to certain chemotherapeutic agents.

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Transformation of mammalian cells by avian myelocytomatosis virus and avian erythroblastosis virus

Cited by 166 publications

References 14 publications

A general method for the generation of high-titer, pantropic retroviral vectors: highly efficient infection of primary hepatocytes.

A general method for the generation of high-titer, pantropic retroviral vectors: highly efficient infection of primary hepatocytes.

Candidate tumor suppressor HYAL2 is a glycosylphosphatidylinositol (GPI)-anchored cell-surface receptor for jaagsiekte sheep retrovirus, the envelope protein of which mediates oncogenic transformation

Susceptibility to apoptosis is differentially regulated by c-myc and mutated Ha-ras oncogenes and is associated with endonuclease availability

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