Document Detail

The PTEN tumor suppressor inhibits human airway smooth muscle cell migration.
MedLine Citation:
PMID:  21042784     Owner:  NLM     Status:  MEDLINE    
Airway remodeling in asthma is characterized by increased airway smooth muscle (ASM) mass, accompanied by cell migration. It is well known that the proliferation and migration of ASM cells (ASMCs) play a key role in airway remodeling, but the precise mechanism modulating these cellular events remains unclear. One of the genes most likely to be involved in this process is the phosphatase and tensin homolog (PTEN) gene, whose deletion from chromosome 10 can inhibit the proliferation and migration of many cell types. In this study, we investigated the effects of PTEN on human ASMCs. The cells were infected with recombinant adenovirus containing wild-type PTEN cDNA (Ad-PTEN), and the results were compared with those from the uninfected cells and those infected with the GFP-labeled adenovirus vector. Cell proliferation was measured using the MTT method. Cell migration was determined by wound-healing and transwell assays. The expressions of PTEN, phospho-Akt, Akt, phospho-ERK1/2, ERK1/2, phospho-focal adhesion kinase (FAK) and FAK, were examined by Western blot analysis. The results show that PTEN is expressed endogenously in ASMCs, and that Ad-PTEN inhibits the proliferation and migration of these cells. In addition, the Ad-PTEN treatment decreased the phosphorylation of Akt and FAK but not that of ERK1/2. In conclusion, this study demonstrates that PTEN overexpression inhibits the proliferation and migration of human ASMCs by down-regulating the activity of the Akt and FAK signaling pathways.
Haibing Lan; Haohai Zhong; Yang Gao; Dunqiang Ren; Lili Chen; Dacheng Zhang; Wenyan Lai; Jian Xu; Yaling Luo
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  International journal of molecular medicine     Volume:  26     ISSN:  1791-244X     ISO Abbreviation:  Int. J. Mol. Med.     Publication Date:  2010 Dec 
Date Detail:
Created Date:  2010-11-02     Completed Date:  2011-03-08     Revised Date:  2012-06-05    
Medline Journal Info:
Nlm Unique ID:  9810955     Medline TA:  Int J Mol Med     Country:  Greece    
Other Details:
Languages:  eng     Pagination:  893-9     Citation Subset:  IM    
Department of Respiratory Diseases, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, P.R. China.
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MeSH Terms
Actins / metabolism
Bronchi / cytology
Cell Migration Assays
Cell Movement / physiology*
Cell Proliferation
Cells, Cultured
Cytoskeleton / metabolism
Electrophoresis, Polyacrylamide Gel
Extracellular Signal-Regulated MAP Kinases / metabolism
Focal Adhesion Kinase 1 / metabolism
MAP Kinase Signaling System
Myocytes, Smooth Muscle / cytology,  metabolism,  physiology*
PTEN Phosphohydrolase / biosynthesis*,  genetics
Proto-Oncogene Proteins c-akt / metabolism
Signal Transduction
Reg. No./Substance:
0/Actins; EC Adhesion Kinase 1; EC protein, human; EC Proteins c-akt; EC Signal-Regulated MAP Kinases; EC protein, human; EC Phosphohydrolase

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