Analyses of cross talk between cell proliferation and autophagyregulated by the MLF1-CSN-COP1-p53 pathway

我们通过白血病相关的MLF 1-CSN-COP 1-p53通路分析了细胞周期抑制和自噬之间的串扰，其中中心调节因子是E3泛素连接酶COP 1。我们发现，COP 1显着抑制DNA损伤诱导的自噬（紫外线照射）导致肿瘤的发生，并与FIP 200，自噬促进因子相互作用。这些数据表明，MLF 1-CSN-COP 1-p53通路通过控制细胞周期和自噬之间的调节而有助于肿瘤发生。

We analyzed cross talk between cell cycle inhibition and autophagy through a leukemia-associated MLF1-CSN-COP1-p53 pathway, in which the center regulator is the E3 ubiquitin ligase COP1. We found that COP1 markedly inhibits DNA damage-induced (UV irradiation) autophagy leading to tumorigenesis and interacts with FIP200, an autophagy-promoting factor. These data suggest that the MLF1-CSN-COP1-p53 pathway contributes to tumorigenesis by controlling the regulation between cell cycle and autophagy.