Source:http://linkedlifedata.com/resource/pubmed/id/19913389
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
2010-2-3
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pubmed:abstractText |
alpha-actinin-4, originally identified as an actin-binding protein associated with cell motility, invasion, and metastasis of cancer cells, appears to be overexpressed in various human epithelial carcinomas, including colorectal, breast, esophageal, ovarian, and non-small cell lung carcinomas. The authors evaluated whether alpha-actinin-4 might be appropriate as a molecular target for cancer gene therapy. In 64 primary oral squamous cell carcinomas (OSCCs) and 10 normal oral mucosal specimens, and in seven human OSCC cell lines, alpha-actinin-4 expression was evaluated immunologically and correlations with clinicopathologic factors were examined. Overexpression of alpha-actinin-4 was detected in 38 of 64 oral squamous cell carcinomas (70%); significantly more frequently than in normal oral mucosa. The expression of alpha-actinin-4 was significantly associated with invasion potential defined by the Matrigel invasion assay. Cancer cell lines with higher alpha-actinin-4 expression had greater invasive potential. An RNAi-mediated decrease in alpha-actinin-4 expression reduced the invasion potential. These results indicated that the overexpression of alpha-actinin-4 was associated with an aggressive phenotype of OSCC. The study indicated that alpha-actinin-4 could be a potential molecular target for gene therapy by RNAi targeting for OSCC.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
D
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
1399-0020
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pubmed:author | |
pubmed:copyrightInfo |
Copyright 2009 International Association of Oral and Maxillofacial Surgeons. Published by Elsevier Ltd. All rights reserved.
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pubmed:issnType |
Electronic
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pubmed:volume |
39
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
61-7
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pubmed:meshHeading |
pubmed-meshheading:19913389-Actinin,
pubmed-meshheading:19913389-Blotting, Western,
pubmed-meshheading:19913389-Carcinoma, Squamous Cell,
pubmed-meshheading:19913389-Cell Line, Tumor,
pubmed-meshheading:19913389-Cell Nucleus,
pubmed-meshheading:19913389-Cytoplasm,
pubmed-meshheading:19913389-Diffusion Chambers, Culture,
pubmed-meshheading:19913389-Down-Regulation,
pubmed-meshheading:19913389-Female,
pubmed-meshheading:19913389-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:19913389-Gene Knockdown Techniques,
pubmed-meshheading:19913389-Humans,
pubmed-meshheading:19913389-Immunohistochemistry,
pubmed-meshheading:19913389-Keratinocytes,
pubmed-meshheading:19913389-Male,
pubmed-meshheading:19913389-Middle Aged,
pubmed-meshheading:19913389-Mouth Mucosa,
pubmed-meshheading:19913389-Mouth Neoplasms,
pubmed-meshheading:19913389-Neoplasm Invasiveness,
pubmed-meshheading:19913389-Neoplasm Staging,
pubmed-meshheading:19913389-Phenotype,
pubmed-meshheading:19913389-RNA, Small Interfering,
pubmed-meshheading:19913389-RNA Interference,
pubmed-meshheading:19913389-Reverse Transcriptase Polymerase Chain Reaction
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pubmed:year |
2010
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pubmed:articleTitle |
RNAi-mediated down-regulation of alpha-actinin-4 decreases invasion potential in oral squamous cell carcinoma.
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pubmed:affiliation |
Department of Oral and Maxillofacial Surgery, Unit of Translational Medicine, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan. shinshin@nagasaki-u.ac.jp
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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