Fos expression induces growth arrest in tumorigenic neuroretina cells
| Autor: | C, Garrido, S, Plaza, D, Gospodarowicz, S, Saule |
|---|---|
| Rok vydání: | 1993 |
| Předmět: |
Receptors
Thyroid Hormone Proto-Oncogene Proteins c-jun Chick Embryo Transfection Retina Cell Transformation Neoplastic Phenotype Retroviridae Proviruses Proto-Oncogene Proteins Cell Adhesion Animals Fibroblast Growth Factor 2 RNA Messenger Growth Substances Proto-Oncogene Proteins c-fos Cell Division |
| Zdroj: | Oncogene. 8(10) |
| ISSN: | 0950-9232 |
| Popis: | E26-infected chicken neuroretina (CNR) cells expressing P135gag-myb-ets are non-transformed and growth can be stimulated by basic fibroblast growth factor (bFGF). In contrast, MHE226-infected CNR cells, which express p61/63myc in addition to the P135gag-myb-ets of E26, are transformed, tumorigenic cells and are growth inhibited by bFGF. We looked for differences in both cells types which could help to understand the molecular basis of the bFGF response. We found marked differences in c-fos expression. In MHE226-CNR cells c-fos mRNA was induced by 12-O-tetradecanoyl phorbol 13-acetate (TPA) and bFGF, both inhibitors of MHE226-infected cell growth. In contrast, serum, a strong growth inducer, did not stimulate c-fos expression. In E26-infected cells all of these factors induced cell growth and c-fos expression. MHE226-CNR cells superinfected with v-fosFBJ-expressing retrovirus were inhibited in their growth and unresponsive to bFGF. Introduction of v-fosFBJ in E26 CNR cells transformed them but they remained sensitive to bFGF. These results suggest that fos is involved in the induced growth arrest of MHE226-CNR cells. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|