Molecular mechanism of cellular senescence in oral precancerous

细胞衰老是一种不可逆转的细胞周期停滞形式，被认为是防止肿瘤发生的重要保障。然而，在很大程度上仍不清楚细胞周期停滞的不可逆性是如何在细胞衰老中建立的。在这里，我们发现，活性氧物种(ROS)的持续产生对于细胞衰老的不可逆性是必不可少的，并且有几个基因参与了这一机制。此外，我们还鉴定了一系列受ROS激活的蛋白酶体依赖的蛋白降解途径控制的蛋白质。这些结果揭示了一条调控细胞衰老不可逆性的新途径。

Cellular senescence, an irreversible form of cell cycle arrest, is known to be acting as an important safeguard against neoplasia. However, it remains largely unclear how irreversibility of cell cycle arrest is established in cellular senescence. Here, we discovered that continuous production of reactive oxygen species (ROS) is essential for irreversibility of cellular senescence and that several genes are involved in this mechanism. Furthermore, we identified a series of proteins controlled by a proteasomal-dependent protein degradation pathway activated by ROS. These results unveil a novel pathway regulating the irreversibility of cellular senescence.