Ling S B, Sun D G, Tang B, Guo C, Zhang Y, Liang R, Wang L M
Department of General Surgery, The Second Affiliated Hospital of Dalian Medical University, Dalian, China.
Cell Mol Biol (Noisy-le-grand). 2012 Dec 5;58 Suppl:OL1803-8.
The Ubiquitin--specific protease 22 (USP22) is a new putative cancer stem cell marker, which plays a significant role in tumorigenesis and cell--cycle progression. However, little is known about the impact of USP22 knock--down on the growth of human hepatoma cell lines. In this study, elevated expression of USP22 was observed in the human HepG2 hepatic cancer cell line compared to the normal human hepatocyte Chang liver cell line. Subsequently, we used siRNA specifically suppressing expression of USP22 and observed that the knock--down of USP22 could effectively induce cell cycle arrest and inhibit HepG2 cell proliferation. Furthermore, our results showed that USP22 deletion caused down--regulation of cyclin D2 expression and up--regulation of p15 and p21 expression. Collectively, Our findings indicate that USP22 may be responsible for HepG2 cell growth and USP22 regulates the cell cycle via the c--Myc/cyclin D2 pathway and down--regulating p15 and p21 expression in HepG2 cell.
泛素特异性蛋白酶22（USP22）是一种新的假定癌症干细胞标志物，在肿瘤发生和细胞周期进程中发挥重要作用。然而，关于USP22基因敲低对人肝癌细胞系生长的影响知之甚少。在本研究中，与正常人肝细胞Chang liver细胞系相比，在人HepG2肝癌细胞系中观察到USP22表达升高。随后，我们使用特异性抑制USP22表达的小干扰RNA（siRNA），观察到USP22基因敲低可有效诱导细胞周期停滞并抑制HepG2细胞增殖。此外，我们的结果表明，USP22缺失导致细胞周期蛋白D2表达下调以及p15和p21表达上调。总体而言，我们的研究结果表明，USP22可能与人HepG2细胞生长有关，并且USP22通过c-Myc/细胞周期蛋白D2途径以及下调HepG2细胞中p15和p21的表达来调节细胞周期。
