Document Detail

Inhibition of epithelial to mesenchymal transition in metastatic breast carcinoma cells by c-Src suppression.
MedLine Citation:
PMID:  20705589     Owner:  NLM     Status:  MEDLINE    
The aberrant activation of c-Src regulates multiple functions during tumor progression. This study was conducted to investigate the role of c-Src suppression in epithelial to mesenchymal transition (EMT) process in human breast carcinoma cells. c-Src suppression by PP2 (a Src-family kinase inhibitor) or small interfering RNA (siRNA) was carried out in MCF-7 and MDA-MB-231 cells. Cell migration was analyzed by wound-healing assay. The transcription and protein levels of EMT markers and transcription factors were evaluated by reverse transcription-PCR and Western blot analysis, respectively. The changed cell morphology was photographed by light microscope. c-Src suppression by PP2 or siRNA reversed the mesenchymal-like phenotype in MDA-MB-231 cells. E-cadherin was upregulated in MCF-7 and MDA-MB-231 cells after c-Src suppression, whereas vimentin was downregulated in MDA-MB-231 cells. Slug and SIP1 were downregulated after c-Src suppression in MCF-7 and MDA-MB-231 cells, whereas Twist was unchanged. These results suggest that c-Src suppression by PP2 or siRNA may inhibit EMT through regulation of different transcription factors in breast carcinoma cells that have different metastatic potential.
Xiang Liu; Renqing Feng
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-06-10
Journal Detail:
Title:  Acta biochimica et biophysica Sinica     Volume:  42     ISSN:  1745-7270     ISO Abbreviation:  Acta Biochim. Biophys. Sin. (Shanghai)     Publication Date:  2010 Jul 
Date Detail:
Created Date:  2010-08-13     Completed Date:  2010-11-29     Revised Date:  2011-09-28    
Medline Journal Info:
Nlm Unique ID:  101206716     Medline TA:  Acta Biochim Biophys Sin (Shanghai)     Country:  China    
Other Details:
Languages:  eng     Pagination:  496-501     Citation Subset:  IM    
Peking University, Beijing, China.
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MeSH Terms
Blotting, Western
Breast Neoplasms / genetics,  metabolism,  pathology
Cadherins / genetics,  metabolism
Cell Line
Cell Line, Tumor
Cell Movement / drug effects
Epithelial Cells / metabolism*,  pathology
Mesoderm / metabolism*,  pathology
Neoplasm Metastasis
Nerve Tissue Proteins / genetics,  metabolism
Pyrimidines / pharmacology
RNA Interference
RNA-Binding Proteins / genetics,  metabolism
Reverse Transcriptase Polymerase Chain Reaction
Transcription Factors / genetics,  metabolism
Tumor Markers, Biological / genetics,  metabolism*
Vimentin / genetics,  metabolism
src-Family Kinases / antagonists & inhibitors,  genetics,  metabolism*
Reg. No./Substance:
0/AG 1879; 0/Cadherins; 0/GEMIN2 protein, human; 0/Nerve Tissue Proteins; 0/Pyrimidines; 0/RNA-Binding Proteins; 0/Transcription Factors; 0/Tumor Markers, Biological; 0/Vimentin; 0/snail family transcription factors; EC Kinases

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

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