Source:http://linkedlifedata.com/resource/pubmed/id/16273209
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
2005-11-7
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pubmed:abstractText |
Loss of E-cadherin expression allows carcinoma cells to liberate from the primary site and enhances invasion and metastasis. The genetic aberration of E-cadherin is a rare event in sporadic carcinomas, and transcription repressors are considered to take a central role in E-cadherin loss. However, expression of E-cadherin repressors is largely dependent on tissue and cell type. To identify the repressor expressed in oral squamous carcinomas, we compared the expression levels of E-cadherin and repressors by real-time RT-PCR. Among the repressors including SNAIL, SLUG, SIP1, E12 and E47, SIP1 was inversely correlated to E-cadherin (P < 0.05). Chromatin immunoprecipitation showed that SIP1 specifically bound to the E-cadherin promoter region. SIP1 expression was immuno-histochemically detected in 27.7% of 47 oral carcinomas, and SIP1-positive carcinomas did not express E-cadherin (P < 0.01). Thirteen patients with SIP1 staining showed a lower disease-specific survival rate (P < 0.05). Multivariate risk factor analysis demonstrated that SIP1 expression was an independent prognostic value for disease-specific overall survival (P < 0.05). These results suggest that SIP1 contributes to the loss of E-cadherin expression and that detection of SIP1 expression is a predictive and prognostic tool in clinical management of oral carcinomas.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
1019-6439
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
27
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1535-41
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:16273209-Adult,
pubmed-meshheading:16273209-Aged,
pubmed-meshheading:16273209-Aged, 80 and over,
pubmed-meshheading:16273209-Analysis of Variance,
pubmed-meshheading:16273209-Binding Sites,
pubmed-meshheading:16273209-Cadherins,
pubmed-meshheading:16273209-Carcinoma, Squamous Cell,
pubmed-meshheading:16273209-Cell Line,
pubmed-meshheading:16273209-Cell Line, Tumor,
pubmed-meshheading:16273209-Disease Progression,
pubmed-meshheading:16273209-Female,
pubmed-meshheading:16273209-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:16273209-Homeodomain Proteins,
pubmed-meshheading:16273209-Humans,
pubmed-meshheading:16273209-Immunohistochemistry,
pubmed-meshheading:16273209-Male,
pubmed-meshheading:16273209-Middle Aged,
pubmed-meshheading:16273209-Mouth Neoplasms,
pubmed-meshheading:16273209-Prognosis,
pubmed-meshheading:16273209-Promoter Regions, Genetic,
pubmed-meshheading:16273209-Protein Binding,
pubmed-meshheading:16273209-Repressor Proteins,
pubmed-meshheading:16273209-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:16273209-Survival Analysis
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pubmed:year |
2005
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pubmed:articleTitle |
Expression of SIP1 in oral squamous cell carcinomas: implications for E-cadherin expression and tumor progression.
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pubmed:affiliation |
Department of Biochemistry, School of Dentistry at Tokyo, The Nippon Dental University, Tokyo, Japan.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
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