The dark side of E2F1: in transit beyond apoptosis.
E2F1 plays a critical role in cell-cycle progression and the induction of apoptosis in response to DNA damage. The latest evidence has uncovered that this tumor suppressor is most relevant for cancer progression and chemoresistance. Increased abundance of E2F1 triggers invasion and metastasis by activating growth receptor signaling pathways, which in turn promote an antiapoptotic tumor environment. The data shed light on the molecular mechanisms underlying E2F1-induced prometastatic activity and predict its radical switch from a mediator of cell death toward an accelerator of tumor progression. This raises the perspective of new drug targets at late-stage cancer.
Department of Vectorology and Experimental Gene Therapy, Biomedical Research Center, University of Rostock, Rostock, Germany.
David
D
Engelmann
Brigitte M
BM
Pützer
D017209:Apoptosis / Q000502:physiology*; D018450:Disease Progression; D019008:Drug Resistance, Neoplasm; D050687:E2F1 Transcription Factor / Q000502:physiology*; D006801:Humans; D008954:Models, Biological; D009361:Neoplasm Invasiveness; D009362:Neoplasm Metastasis; D009369:Neoplasms / Q000473:pathology / Q000503:physiopathology*; D025521:Tumor Suppressor Proteins / Q000502:physiology*
D050687:E2F1 Transcription Factor; D025521:Tumor Suppressor Proteins