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Vol. 18, Issue 7, 2630-2635, July 2007

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Depletion of the Nucleolar Protein Nucleostemin Causes G1 Cell Cycle Arrest via the p53 Pathway

Program in Cell Dynamics and Department of Biochemistry and Molecular Pharmacology, University of Massachusetts Medical School, Worcester, MA 01605

Submitted March 16, 2007; Revised April 19, 2007; Accepted April 26, 2007
Monitoring Editor: Mark Solomon

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.

The online version of this article contains supplemental material at MBC Online (http://www.molbiolcell.org).

Address correspondence to: Hanhui Ma (hanhui.ma{at}umassmed.edu) or Thoru Pederson (thoru.pederson{at}umassmed.edu)

Abbreviations used: NS, nucleostemin; ARF, alternate reading frame.