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Brief Report

E2F1 plays a direct role in Rb stabilization and p53-independent tumor suppression

Gustavo Palacios, Flaminia Talos, Alice Nemajerova, Ute M. Moll and Oleksi Petrenko

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To better understand the role of E2F1 in tumor formation, we analyzed spontaneous tumorigenesis in p53-/-E2F1+/+ and p53-/-E2F1-/- mice. We show that the combined loss of p53 and E2F1 leads to an increased incidence of sarcomas and carcinomas compared to the loss of p53 alone. E2F1-deficient tumors show wide chromosomal variation, indicative of genomic instability. Consistent with this, p53-/-E2F1-/- primary fibroblasts have a reduced capacity to maintain genomic stability when exposed to S-phase inhibitors or genotoxic drugs. A major mechanism of E2F1’s contribution to genomic integrity lies in mediating stabilization and engagement of the Rb protein.

Authors

Gustavo Palacios

State University of New York at Stony Brook; Stony Brook, NY

Flaminia Talos

State University of New York at Stony Brook; Stony Brook, NY

Alice Nemajerova

State University of New York at Stony Brook; Stony Brook, NY

Ute M. Moll

Stony Brook University; Stony Brook, NY

Oleksi Petrenko

State University of New York at Stony Brook; Stony Brook, NY

Purchase article for $19

Subscribe to this journal for $129/year