Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences-Shanghai Jiao Tong University School of Medicine (SJTU-SM), Shanghai, China.
Cancer Lett. 2011 Oct 1;309(1):78-84. doi: 10.1016/j.canlet.2011.05.019. Epub 2011 Jun 12.
SUMO conjugation emerges as an important mechanism in regulating protein localization, stability and activity. SUMOylation is a dynamic process and can be reversed by a family of sentrin/SUMO-specific proteases (SENPs). However, the biological roles of SENPs in cellular processes are largely unknown. Here, we show that SENP1, a member of SENP family, is overexpressed in most of colon cancer tissues. Silencing of SENP1 expression inhibits cell growth with G(1) arrest in vitro and in nude mice and colony formation in colon cancer cell line DLD-1, suggesting that SENP1 is essential for cell growth in the colon cancer cell line. Accordingly, silencing of SENP1 results in upregulation of CDK inhibitors such as p16, p19, p21 and p27. These results suggest that SENP1 might play a role in cell cycle regulation of colon cancer cells.
SUMO 缀合作用是调节蛋白质定位、稳定性和活性的一个重要机制。SUMOylation 是一个动态的过程，可以被一系列的 sentrin/SUMO 特异性蛋白酶 (SENPs) 逆转。然而，SENPs 在细胞过程中的生物学作用在很大程度上是未知的。在这里，我们表明 SENP1，SENP 家族的一员，在大多数结肠癌组织中过度表达。SENP1 表达的沉默抑制了体外和裸鼠中细胞的生长，并抑制了结肠癌细胞系 DLD-1 的集落形成，表明 SENP1 对于结肠癌细胞的生长是必需的。因此，沉默 SENP1 导致 CDK 抑制剂如 p16、p19、p21 和 p27 的上调。这些结果表明，SENP1 可能在结肠癌细胞的细胞周期调控中发挥作用。
