Department of Vectorology and Experimental Gene Therapy, Biomedical Research Center, University of Rostock, Rostock, Germany.
Cancer Res. 2012 Feb 1;72(3):571-5. doi: 10.1158/0008-5472.CAN-11-2575.
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.
E2F1 在细胞周期进程中发挥着关键作用，并能诱导细胞凋亡以响应 DNA 损伤。最新证据表明，这种肿瘤抑制因子与癌症的进展和化疗耐药性最为相关。E2F1 的丰度增加会通过激活生长受体信号通路来引发侵袭和转移，进而促进抗凋亡的肿瘤微环境。这些数据揭示了 E2F1 诱导的促转移活性的分子机制，并预测其从细胞死亡的介导者向肿瘤进展的加速剂的根本转变。这为晚期癌症的新药物靶点提供了新的视角。
