| The role of serum response factor in hepatocellular carcinoma: implications for disease progression. | |
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MedLine Citation:
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PMID: 20811705 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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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:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: International journal of oncology Volume: 37 ISSN: 1791-2423 ISO Abbreviation: Int. J. Oncol. Publication Date: 2010 Oct |
Date Detail:
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Created Date: 2010-09-02 Completed Date: 2010-12-23 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 9306042 Medline TA: Int J Oncol Country: Greece |
Other Details:
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Languages: eng Pagination: 837-44 Citation Subset: IM |
Affiliation:
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Department of Pathology, Chonbuk National University, Medical School, Institute for Medical Sciences, Research Institute of Clinical Medicine, Jeonju, Chonbuk 561-756, Korea. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Actins
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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 Humans Liver Neoplasms / genetics, metabolism*, pathology Neoplasm Invasiveness RNA Interference Serum Response Factor / genetics, metabolism* Transfection Vimentin / metabolism Wnt Proteins / metabolism beta Catenin / metabolism rhoA GTP-Binding Protein / metabolism |
| Chemical | |
Reg. No./Substance:
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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 3.6.5.2/rhoA GTP-Binding Protein |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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