Document Detail

The role of serum response factor in hepatocellular carcinoma: implications for disease progression.
MedLine Citation:
PMID:  20811705     Owner:  NLM     Status:  MEDLINE    
Serum response factor (SRF) regulates transcription of the immediate early genes and triggers proliferation, migration and differentiation in several types of cells. We examined the role of SRF in HCC by transfecting the SRF cDNA in HLE cells and the SRF anti-sense cDNA in sarcomatoid HCC cells. The overexpression of SRF in the HLE cells significantly increased the cell growth and proliferation. Overexpression of SRF increased actin polymerization of the HCC cells and induced morphologic changes. The mesenchymal markers vimentin, N-cadherin and RhoA were highly expressed in the SRF-transfected HLE cells. Furthermore, the overexpression of SRF in the HLE cells increased the expression levels of the active form of the beta-catenin and Wnt/beta-catenin target genes, such as c-myc and cyclin D1. The overexpression of SRF significantly enhanced the cell migration and invasiveness of HCC cells. Conversely, inhibition of the SRF expression in the sarcomatoid SH-J1 cells by the SRF anti-sense cDNA significantly decreased migration and invasion through the attenuated expression of mesenchymal markers and the proteins involved in the Wnt/beta-catenin pathway. These results indicate that the overexpression of SRF in HCC cells modulates the Wnt/beta-catenin pathway, and this plays an important role in HCC progression.
Chang Young Kwon; Kyung Ryoul Kim; Ha Na Choi; Myoung Ja Chung; Sang Jae Noh; Dae Ghon Kim; Myoung Jae Kang; Dong Geun Lee; Woo Sung Moon
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  International journal of oncology     Volume:  37     ISSN:  1791-2423     ISO Abbreviation:  Int. J. Oncol.     Publication Date:  2010 Oct 
Date Detail:
Created Date:  2010-09-02     Completed Date:  2010-12-23     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9306042     Medline TA:  Int J Oncol     Country:  Greece    
Other Details:
Languages:  eng     Pagination:  837-44     Citation Subset:  IM    
Department of Pathology, Chonbuk National University, Medical School, Institute for Medical Sciences, Research Institute of Clinical Medicine, Jeonju, Chonbuk 561-756, Korea.
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MeSH Terms
Actins / metabolism
Antigens, CD / metabolism
Cadherins / metabolism
Carcinoma, Hepatocellular / genetics,  metabolism*,  pathology
Cell Line, Tumor
Cell Movement
Cell Proliferation
Cell Shape
Disease Progression
Epithelial-Mesenchymal Transition
Gene Expression Regulation, Neoplastic
Genes, Immediate-Early
Liver Neoplasms / genetics,  metabolism*,  pathology
Neoplasm Invasiveness
RNA Interference
Serum Response Factor / genetics,  metabolism*
Vimentin / metabolism
Wnt Proteins / metabolism
beta Catenin / metabolism
rhoA GTP-Binding Protein / metabolism
Reg. No./Substance:
0/Actins; 0/Antigens, CD; 0/CDH2 protein, human; 0/CTNNB1 protein, human; 0/Cadherins; 0/SRF protein, human; 0/Serum Response Factor; 0/Vimentin; 0/Wnt Proteins; 0/beta Catenin; 124671-05-2/RHOA protein, human; EC GTP-Binding Protein

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