Document Detail


Inhibition of centriole duplication by centrobin depletion leads to p38-p53 mediated cell-cycle arrest.
MedLine Citation:
PMID:  20085806     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Previously, we have identified a novel centrosomal protein centrobin that asymmetrically localizes to the daughter centriole. We found that depletion of centrobin expression inhibited the centriole duplication and impaired cytokinesis. However, the biological significance of centrobin in the cell cycle remains unknown. In the current study, we observed that silencing centrobin significantly inhibited the proliferation of lung cancer cell A549 and prevented the cells from G1 to S transition, whereas the growth rate of lung cancer cell line H1299, a p53-null cell line, was not affected. Furthermore, we demonstrated that the G1-S-phase arrest induced by centrobin knockdown in A549 cells is mediated by the upregulation of cell-cycle regulator p53, which is associated with the activation of cellular stress induced p38 pathway instead of DNA damage induced ATM pathway. Inhibition of p38 activity or downregulation of p38 expression could overcome the cell-cycle arrest caused by centrobin depletion. Taken together, our current findings demonstrated that centrobin plays an important role in the progression of cell cycle, and a tight association between the cell-cycle progression and defective centrosomes caused by depletion of centrobin.
Authors:
Libing Song; Ting Dai; Huaping Xiong; Chuyong Lin; Huanxin Lin; Tingting Shi; Jun Li
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-01-18
Journal Detail:
Title:  Cellular signalling     Volume:  22     ISSN:  1873-3913     ISO Abbreviation:  Cell. Signal.     Publication Date:  2010 May 
Date Detail:
Created Date:  2010-02-22     Completed Date:  2010-05-05     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8904683     Medline TA:  Cell Signal     Country:  England    
Other Details:
Languages:  eng     Pagination:  857-64     Citation Subset:  IM    
Copyright Information:
2010 Elsevier Inc. All rights reserved.
Affiliation:
Sun Yat-sen University Cancer Center, Guangzhou, Guangdong, China. lb.song1@gmail.com
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MeSH Terms
Descriptor/Qualifier:
Bromodeoxyuridine / metabolism
Cell Count
Cell Cycle*
Cell Cycle Proteins / metabolism*
Cell Line, Tumor
Cell Proliferation
Centrioles / enzymology*
G1 Phase
Gene Knockdown Techniques
Humans
Ki-67 Antigen / metabolism
S Phase
Signal Transduction
Tumor Suppressor Protein p53 / metabolism*
p38 Mitogen-Activated Protein Kinases / metabolism*
Chemical
Reg. No./Substance:
0/CNTROB protein, human; 0/Cell Cycle Proteins; 0/Ki-67 Antigen; 0/Tumor Suppressor Protein p53; 59-14-3/Bromodeoxyuridine; EC 2.7.11.24/p38 Mitogen-Activated Protein Kinases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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