A Swiss 3T3 variant cell line resistant to the effects of tumor promoters cannot be transformed by src
| Autor: | M Nori, L K Shawver, Michael J. Weber |
|---|---|
| Rok vydání: | 1990 |
| Předmět: |
DNA Replication
Drug Resistance Deoxyglucose Biology Transfection medicine.disease_cause Oncogene Protein pp60(v-src) Mice Plasmid Retrovirus medicine Animals Molecular Biology Cells Cultured Epidermal Growth Factor Oncogene Oncogenes Cell Biology biology.organism_classification Molecular biology Transformation (genetics) Cell Transformation Neoplastic Retroviridae Cell culture Tetradecanoylphorbol Acetate DNA Probes Carcinogenesis Research Article Plasmids Proto-oncogene tyrosine-protein kinase Src |
| Zdroj: | Molecular and Cellular Biology. 10:4155-4162 |
| ISSN: | 1098-5549 0270-7306 |
| Popis: | To study the relationship between oncogenesis by v-src and normal cellular signalling pathways, we determined the effects of v-src on 3T3-TNR9 cells, a Swiss 3T3 variant which does not respond mitogenically to tumor promoters such as 12-O-tetradecanoyl-phorbol-13-acetate (TPA). We found that src was unable to transform these variant cells, whether the oncogene was introduced by infection with a murine retrovirus vector or by transfection with plasmid DNA. 3T3-TNR9 cells were not inherently resistant to transformation, since infection with similar recombinant retroviruses containing either v-ras or v-abl did induce transformation. Further analysis of Swiss 3T3 and 3T3-TNR9 cell populations infected with the v-src-containing retrovirus revealed that although the amount of v-src DNA in each was approximately the same, the level of the v-src message and protein and the overall level of phosphotyrosine expressed in the infected variants was much less than in infected parental cells. Cotransfection experiments using separate v-src and neo plasmids revealed a decrease in the number of G418-resistant colonies when transfections of TNR9 cells occurred in the presence of the src-containing plasmid, suggesting a growth inhibitory effect of v-src on 3T3-TNR9 cells, as has also been found for TPA itself. Since v-src cannot transform this variant cell line, which does not respond mitogenically to the protein kinase C agonist TPA, we suggest that src makes use of the protein kinase C pathway as part of its signalling activities. |
| Databáze: | OpenAIRE |
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