Depletion of the nucleolar protein nucleostemin causes g1 cell cycle arrest via the p53 pathway
Depletion of the nucleolar protein nucleostemin causes g1 cell cycle arrest via the p53 pathway
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DOI：
10.1091/mbc.e07-03-0244
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发表时间：
2007-07-01
影响因子：
3.3
通讯作者：
Pederson, Thoru
中科院分区：
文献类型：
--
作者：
Ma, Hanhui;Pederson, Thoru
核干素(NS)是一种核仁蛋白，表达于成人和胚胎来源的干细胞、转化细胞系和肿瘤中。当增殖细胞退出细胞周期时，NS减少，但目前尚不清楚NS是如何控制的，以及它如何参与细胞生长调节。在这里，我们表明NS被肿瘤抑制因子p14(ARF)下调，而NS基因敲除上调了肿瘤抑制因子P53的水平。NS基因敲除导致P53阳性细胞的G1期细胞周期停滞，但在P53基因缺陷或被小干扰RNA敲除而耗尽的细胞中则没有。这些结果表明，在所研究的细胞中，NS的水平受p14(ARF)的调节，并且NS对G1/S转变的控制是以P53依赖的方式进行的。
Nucleostemin (NS) is a nucleolar protein expressed in adult and embryo-derived stem cells, transformed cell lines, and tumors. NS decreases when proliferating cells exit the cell cycle, but it is unknown how NS is controlled, and how it participates in cell growth regulation. Here, we show that NS is down-regulated by the tumor suppressor p14(ARF) and that NS knockdown elevates the level of tumor suppressor p53. NS knockdown led to G1 cell cycle arrest in p53-positive cells but not in cells in which p53 was genetically deficient or depleted by small interfering RNA knockdown. These results demonstrate that, in the cells investigated, the level of NS is regulated by p14(ARF) and the control of the G1/S transition by NS operates in a p53-dependent manner.