Source:http://linkedlifedata.com/resource/pubmed/id/19428110
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
10
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| pubmed:dateCreated |
2009-5-20
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| pubmed:abstractText |
Malignant transformation of hepatocytes is frequently associated with upregulation of HLA-A expression. Currently there is no information available regarding the mechanisms underlying this phenotypic change. We investigated HLA-A expression in 165 paraffin embedded tissues and 21 fresh tissues from liver cancer patients. Utilizing truncated HLA-A promoter-reporter constructs and gel-shift assay we had identified the regulatory elements and transcription factors required for HLA-A upregulation. 54% of the paraffin embedded tissues showed increased HLA-A expression in their cancerous part. 43% of the fresh liver cancer tissues had increased HLA-A complex expression with the HLA-A heavy chain gene demonstrating the highest level of upregulation (62%). Enhanced HLA-A expression in the liver cell lines QGY7701 and BEL7402 was found to be mediated by binding of interferon regulatory factor 1 (IRF-1) to interferon stimulated response element, and of nuclear transcription factor p65 binding to enhancer A element in the HLA-A promoter of these cell lines. The in vivo relevance of these findings was indicated by the association of the enhanced expression of IRF-1 and accumulation of nuclear p65 with HLA-A upregulation in 8 of the 21 liver cancer lesions investigated. Our results indicated that HLA-A upregulation in liver cancer was mediated by both increased nuclear aggregation of transcription factor p65 and upregulation of transcription factor IRF-1.
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| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Jun
|
| pubmed:issn |
1872-9142
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| pubmed:author | |
| pubmed:issnType |
Electronic
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| pubmed:volume |
46
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
2045-53
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| pubmed:dateRevised |
2009-6-16
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| pubmed:meshHeading |
pubmed-meshheading:19428110-Adult,
pubmed-meshheading:19428110-Aged,
pubmed-meshheading:19428110-Aged, 80 and over,
pubmed-meshheading:19428110-Animals,
pubmed-meshheading:19428110-Antigen Presentation,
pubmed-meshheading:19428110-Carcinoma, Hepatocellular,
pubmed-meshheading:19428110-Cell Line, Tumor,
pubmed-meshheading:19428110-Female,
pubmed-meshheading:19428110-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:19428110-HLA-A Antigens,
pubmed-meshheading:19428110-Humans,
pubmed-meshheading:19428110-Interferon Regulatory Factor-1,
pubmed-meshheading:19428110-Liver Neoplasms,
pubmed-meshheading:19428110-Male,
pubmed-meshheading:19428110-Middle Aged,
pubmed-meshheading:19428110-Protein Binding,
pubmed-meshheading:19428110-Response Elements,
pubmed-meshheading:19428110-Transcription Factor RelA,
pubmed-meshheading:19428110-Up-Regulation
|
| pubmed:year |
2009
|
| pubmed:articleTitle |
IRF-1 and p65 mediate upregulation of constitutive HLA-A antigen expression by hepatocellular carcinoma cells.
|
| pubmed:affiliation |
The Key Laboratory of Developmental Genes and Human Disease, Ministry of Education, Department of Genetics and Developmental Biology, Southeast University Medical School, Nanjing, Jiangsu 210009, China.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
|