Department of Pathology & Immunology, Baylor College of Medicine, Texas Children's Hospital, Houston, TX 77030, USA.
Department of Pediatrics, Baylor College of Medicine, Texas Children's Hospital, Houston, TX 77030, USA.
Leuk Res. 2014 Feb;38(2):210-7. doi: 10.1016/j.leukres.2013.10.006. Epub 2013 Oct 14.
G0/G1 switch gene 2 (G0S2) is a basic protein with ill-defined function that inhibits the proliferation of hematopoietic stem cells. Herein, we show that treatment of K562 cells with 5-azacytidine (5-Aza) resulted in a 24-fold increase in G0S2 expression and a reduction in cell growth. Conversely, gene demethylation in the presence of G0S2-specific shRNA restored proliferation, further supporting an inhibitory role for G0S2 in cell proliferation. Elevated levels of G0S2 inhibited the division of K562 cells by sequestering the nucleolar phosphoprotein nucleolin in the cytosol. G0S2 inhibited the proliferation of leukemia cells in vivo in xenograft models. Collectively, our data identify a new mechanism that controls proliferation in K562 cells, suggesting a possible tumor suppressor function in leukemia cells.
G0/G1 开关基因 2（G0S2）是一种基本蛋白，其功能尚未明确，它能抑制造血干细胞的增殖。在此，我们发现用 5-氮杂胞苷（5-Aza）处理 K562 细胞，可使 G0S2 表达增加 24 倍，细胞生长减少。相反，在存在 G0S2 特异性 shRNA 的情况下进行基因去甲基化，可恢复增殖，进一步支持 G0S2 在细胞增殖中的抑制作用。G0S2 水平升高通过将核仁磷酸蛋白核仁素（nucleolin）隔离在细胞质中，抑制 K562 细胞的分裂。G0S2 在异种移植模型中抑制体内白血病细胞的增殖。总的来说，我们的数据确定了一种控制 K562 细胞增殖的新机制，提示 G0S2 在白血病细胞中可能具有肿瘤抑制功能。
