FEN1-related senescence

在这里，我们通过RNA干扰研究了FEN1消融对p53完整或不完整的不同类型细胞生长的影响。我们发现FEN1消融触发p53突变的T24细胞衰老。然而，将野生型p53转染到这些T24细胞中可以抑制衰老。另一方面，通过干扰FEN1的表达，没有将携带野生型p53的HT116细胞引入衰老；相反，细胞发生了凋亡。相反，在HT116细胞中，p53缺陷在FEN1 siRNA处理后没有出现衰老或凋亡。有趣的是，电离辐射（5Gy）导致使用FEN1 siRNA处理的p53有效HT116细胞衰老。这些结果表明，fen1诱导的衰老是p53依赖的，这一机制可能参与了紫外线诱导的肿瘤发生。

Here we investigated the effects of FEN1 ablation on growth of different cell types with or without intact p53 by using RNA interference. We found that the FEN1 ablation triggers senescence in p53-mutated T24 cells. However, transfection of the wild-type p53 into these T24 cells inhibited the senescence. On the other hand, HT116 cells with the wild-type p53 were not introduced to senescence by interfering FEN1 expression ; instead, the cells underwent apoptosis. Contrary in HT116 cells defective of p53 did not exhibit senescence or apoptosis after FEN1 siRNA treatment. Interestingly, ionizing irradiation(5Gy) caused senescence in p53-dfective HT116 cells that were treated with FEN1 siRNA. These results suggest that FEN1-induced senescence is p53-dependent and imply that this mechanism may be involved in UV-induced tumorigenesis.