Tumor Progression and Oncogene Addiction in a PDGF-B-Induced Model of Gliomagenesis
| Autor: | Paolo Malatesta, Giorgio Corte, Evelina Tutucci, Filippo Calzolari, Irene Appolloni, Marta Terrile, Sara Caviglia |
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| Jazyk: | angličtina |
| Rok vydání: | 2008 |
| Předmět: |
Cancer Research
in vivo tumor model Cellular differentiation Oligodendroglioma Cell Communication Biology Models Biological lcsh:RC254-282 Immediate early protein Immediate-Early Proteins Mice Glioma medicine Btg2 Animals Genes Tumor Suppressor Progenitor cell Tumor Suppressor Proteins Contact inhibition Brain Cell Differentiation Proto-Oncogene Proteins c-sis Oncogene Addiction medicine.disease Flow Cytometry lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens Transplantation Gene Expression Regulation Neoplastic Mice Inbred C57BL Tumor progression Immunology Cancer research Disease Progression Signal Transduction Research Article |
| Zdroj: | Neoplasia: An International Journal for Oncology Research, Vol 10, Iss 12, Pp 1373-1382 (2008) |
| ISSN: | 1522-8002 1476-5586 |
| Popis: | Platelet-derived growth factor B (PDGF-B) overexpression induces gliomas of different grades from murine embryonic neural progenitors. For the first time, we formally demonstrated that PDGF-B-induced neoplasms undergo progression from nontumorigenic low-grade tumors toward highly malignant forms. This result, showing that PDGF-B signaling alone is insufficient to confer malignancy to cells, entails the requirement for further molecular lesions in this process. Our results indicate that one of these lesions is represented by the down-regulation of the oncosuppressor Btg2. By in vivo transplantation assays, we further demonstrate that fully progressed tumors are PDGF-B-addicted because their tumor-propagating ability is lost when the PDGF-B transgene is silenced, whereas it is promptly reacquired after its reactivation. We provide evidence that this oncogene addiction is not caused by the need for PDGF-B as a mitogen but, rather, to the fact that PDGF-B is required to overcome cell-cell contact inhibition and to confer in vivo infiltrating potential on tumor cells. |
| Databáze: | OpenAIRE |
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