E2F1 Has Both Oncogenic and Tumor-Suppressive Properties in a Transgenic Model
Autor: | Angela M. Pierce, Robin Schneider-Broussard, Irma B. Gimenez-Conti, Claudio J. Conti, Jamie Russell, David G. Johnson |
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Rok vydání: | 1999 |
Předmět: |
Male
Genetically modified mouse endocrine system Skin Neoplasms Transgene Apoptosis Cell Cycle Proteins Mice Transgenic Context (language use) Biology medicine.disease_cause Mice Inbred SENCAR Transgenic Model Mice medicine Animals Humans E2F1 Genes Tumor Suppressor Cell Growth and Development Molecular Biology Transcription factor Skin Neoplasms Experimental Oncogenes Cell Biology E2F Transcription Factors DNA-Binding Proteins Keratin 5 Cancer research Tetradecanoylphorbol Acetate Female biological phenomena cell phenomena and immunity Carrier Proteins Carcinogenesis Transcription Factor DP1 E2F1 Transcription Factor Retinoblastoma-Binding Protein 1 Transcription Factors |
Zdroj: | Molecular and Cellular Biology. 19:6408-6414 |
ISSN: | 1098-5549 |
DOI: | 10.1128/mcb.19.9.6408 |
Popis: | Using a transgenic mouse model expressing the E2F1 gene under the control of a keratin 5 (K5) promoter, we previously demonstrated that increased E2F1 activity can promote tumorigenesis by cooperating with either a v-Ha-ras transgene to induce benign skin papillomas or p53 deficiency to induce spontaneous skin carcinomas. We now report that as K5 E2F1 transgenic mice age, they are predisposed to develop spontaneous tumors in a variety of K5-expressing tissues, including the skin, vagina, forestomach, and odontogenic epithelium. On the other hand, K5 E2F1 transgenic mice are found to be resistant to skin tumor development following a two-stage carcinogenesis protocol. Additional experiments suggest that this tumor-suppressive effect of E2F1 occurs at the promotion stage and may involve the induction of apoptosis. These findings demonstrate that increased E2F1 activity can either promote or inhibit tumorigenesis, dependent upon the experimental context. |
Databáze: | OpenAIRE |
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