Deregulated Expression of E2F1 Induces Hyperplasia and Cooperates with Ras in Skin Tumor Development
March 1998
in “
Oncogene
”
Studysummary This study found that transgenic mice overexpressing E2F1 in their epidermis developed skin tumors, confirming in vivo that deregulated E2F1 activity can contribute to tumor development.
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The study investigated the effects of E2F1 overexpression in transgenic mice, revealing that E2F1 induced hyperplasia in the epidermis without inhibiting terminal differentiation. Mice with high E2F1 levels exhibited decreased hair growth due to abnormal apoptosis in hair follicles. Coexpression with a cyclin D1 transgene intensified epidermal hyperplasia and further disrupted hair follicle development, suggesting that hypophosphorylated Rb counteracts E2F1's proliferative and apoptotic effects. Additionally, E2F1 cooperated with a v-Ha-ras transgene to induce skin tumors, demonstrating that deregulated E2F1 activity could contribute to tumor development, confirming in vitro findings in an in vivo context.
