Document Detail


microRNA-21 negatively regulates Cdc25A and cell cycle progression in colon cancer cells.
MedLine Citation:
PMID:  19826040     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
microRNAs (miRNA) are small noncoding RNAs that participate in diverse biological processes by suppressing target gene expression. Altered expression of miR-21 has been reported in cancer. To gain insights into its potential role in tumorigenesis, we generated miR-21 knockout colon cancer cells through gene targeting. Unbiased microarray analysis combined with bioinformatics identified cell cycle regulator Cdc25A as a miR-21 target. miR-21 suppressed Cdc25A expression through a defined sequence in its 3'-untranslated region. We found that miR-21 is induced by serum starvation and DNA damage, negatively regulates G(1)-S transition, and participates in DNA damage-induced G(2)-M checkpoint through down-regulation of Cdc25A. In contrast, miR-21 deficiency did not affect apoptosis induced by a variety of commonly used anticancer agents or cell proliferation under normal cell culture conditions. Furthermore, miR-21 was found to be underexpressed in a subset of Cdc25A-overexpressing colon cancers. Our data show a role of miR-21 in modulating cell cycle progression following stress, providing a novel mechanism of Cdc25A regulation and a potential explanation of miR-21 in tumorigenesis.
Authors:
Peng Wang; Fangdong Zou; Xiaodong Zhang; Hua Li; Austin Dulak; Robert J Tomko; John S Lazo; Zhenghe Wang; Lin Zhang; Jian Yu
Publication Detail:
Type:  Journal Article     Date:  2009-10-13
Journal Detail:
Title:  Cancer research     Volume:  69     ISSN:  1538-7445     ISO Abbreviation:  Cancer Res.     Publication Date:  2009 Oct 
Date Detail:
Created Date:  2009-10-16     Completed Date:  2009-11-24     Revised Date:  2012-04-05    
Medline Journal Info:
Nlm Unique ID:  2984705R     Medline TA:  Cancer Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  8157-65     Citation Subset:  IM    
Affiliation:
Departments of Pathology and Pharmacology, University of Pittsburgh Cancer Institute, Pittsburgh, Pennsylvania, USA.
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MeSH Terms
Descriptor/Qualifier:
Apoptosis
Bromodeoxyuridine / diagnostic use
Cell Cycle*
Cell Proliferation
Colorectal Neoplasms / genetics*,  metabolism,  pathology*
DNA Damage
Gene Expression Profiling
Gene Expression Regulation, Neoplastic*
Humans
Luciferases / metabolism
MicroRNAs / physiology*
Mitotic Index
Oligonucleotide Array Sequence Analysis
RNA, Messenger / genetics,  metabolism
RNA, Small Interfering / pharmacology
Reverse Transcriptase Polymerase Chain Reaction
cdc25 Phosphatases
Grant Support
ID/Acronym/Agency:
R01 CA106348-01/CA/NCI NIH HHS; R01 CA106348-02/CA/NCI NIH HHS; R01 CA106348-03/CA/NCI NIH HHS; R01 CA106348-04/CA/NCI NIH HHS; R01 CA106348-05/CA/NCI NIH HHS; R01 CA121105-01A1/CA/NCI NIH HHS; R01 CA121105-02/CA/NCI NIH HHS; R01 CA121105-03/CA/NCI NIH HHS; R01 CA129829-01A1/CA/NCI NIH HHS; R01 CA129829-02/CA/NCI NIH HHS; R01 CA129829-05/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/MIRN21 microRNA, human; 0/MicroRNAs; 0/RNA, Messenger; 0/RNA, Small Interfering; 59-14-3/Bromodeoxyuridine; EC 1.13.12.-/Luciferases; EC 3.1.3.48/CDC25A protein, human; EC 3.1.3.48/cdc25 Phosphatases

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