| pubmed-article:19913389 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19913389 | lifeskim:mentions | umls-concept:C0035647 | lld:lifeskim |
| pubmed-article:19913389 | lifeskim:mentions | umls-concept:C0007137 | lld:lifeskim |
| pubmed-article:19913389 | lifeskim:mentions | umls-concept:C0442027 | lld:lifeskim |
| pubmed-article:19913389 | lifeskim:mentions | umls-concept:C0013081 | lld:lifeskim |
| pubmed-article:19913389 | lifeskim:mentions | umls-concept:C2699153 | lld:lifeskim |
| pubmed-article:19913389 | lifeskim:mentions | umls-concept:C1269955 | lld:lifeskim |
| pubmed-article:19913389 | lifeskim:mentions | umls-concept:C0547047 | lld:lifeskim |
| pubmed-article:19913389 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:19913389 | pubmed:dateCreated | 2010-2-3 | lld:pubmed |
| pubmed-article:19913389 | 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. | lld:pubmed |
| pubmed-article:19913389 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19913389 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19913389 | pubmed:citationSubset | D | lld:pubmed |
| pubmed-article:19913389 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19913389 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19913389 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19913389 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19913389 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:19913389 | pubmed:issn | 1399-0020 | lld:pubmed |
| pubmed-article:19913389 | pubmed:author | pubmed-author:YoshidaHH | lld:pubmed |
| pubmed-article:19913389 | pubmed:author | pubmed-author:MizunoAA | lld:pubmed |
| pubmed-article:19913389 | pubmed:author | pubmed-author:YamadaSS | lld:pubmed |
| pubmed-article:19913389 | pubmed:author | pubmed-author:YoshitomeMM | lld:pubmed |
| pubmed-article:19913389 | pubmed:author | pubmed-author:KawasakiGG | lld:pubmed |
| pubmed-article:19913389 | pubmed:author | pubmed-author:YanamotoSS | lld:pubmed |
| pubmed-article:19913389 | pubmed:author | pubmed-author:NemotoT KTK | lld:pubmed |
| pubmed-article:19913389 | pubmed:copyrightInfo | Copyright 2009 International Association of Oral and Maxillofacial Surgeons. Published by Elsevier Ltd. All rights reserved. | lld:pubmed |
| pubmed-article:19913389 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:19913389 | pubmed:volume | 39 | lld:pubmed |
| pubmed-article:19913389 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19913389 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19913389 | pubmed:pagination | 61-7 | lld:pubmed |
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| pubmed-article:19913389 | pubmed:year | 2010 | lld:pubmed |
| pubmed-article:19913389 | pubmed:articleTitle | RNAi-mediated down-regulation of alpha-actinin-4 decreases invasion potential in oral squamous cell carcinoma. | lld:pubmed |
| pubmed-article:19913389 | 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 | lld:pubmed |
| pubmed-article:19913389 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:19913389 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| entrez-gene:81 | entrezgene:pubmed | pubmed-article:19913389 | lld:entrezgene |
| http://linkedlifedata.com/r... | entrezgene:pubmed | pubmed-article:19913389 | lld:entrezgene |
