The E2F family of transcription factors plays an essential role in promoting cell cycle progression, and one member of the family, E2F-1, is also capable of inducting apoptosis. We show here that E2F-1 can induce apoptosis by a death receptor-dependent mechanism, by downregulating TRAF2 protein levels and inhibiting activation of antiapoptotic signals including NF-κB. In this way, E2F-1 expression can lead to the sensitization of cells to apoptosis by a number of agents independently of p53. Deregulation of E2F-1 activity occurs in the majority of human tumors, and the ability of E2F-1 to inhibit antiapoptotic signaling may contribute to the enhanced sensitivity of transformed cells to chemotherapeutic agents.
Phillips, A. C., Ernst, M. K., Bates, S., Rice, N. R., & Vousden, K. H. (1999). E2F-1 Potentiates cell death by blocking antiapoptotic signaling pathways. Molecular Cell, 4(5), 771–781. https://doi.org/10.1016/S1097-2765(00)80387-1