Source:http://linkedlifedata.com/resource/pubmed/id/17393110
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1
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| pubmed:dateCreated |
2007-3-29
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| pubmed:abstractText |
The evolution of hepatocellular carcinoma (HCC) is a compound process which involves many kinds of genes and transductional pathways. The expression of the peptidyl-proplyl-isomerase PIN1 gene, the mutation in exon 3 of beta-catenin and its correspondent abnormal expression and their roles in the hepatocellular carcinogeneisis were investigated. Among 29 pair cases of HCC and non-carcinoma tissues, the expression of PIN1 gene was detected by immunochemical staining. Mutations in exon 3 of beta-catenin gene and differential expression of beta-catenin gene were investigated by the methods of PCR-SSCP, direct sequencing and immunohistochemical technique as well. The results indicated: (1) 44.8% (13/29) cases of HCC presented higher level of PIN1 gene expression than non-cancerous tissues (chi2=32.63, P<0.05), especially in cytoplasm and nucleus, while there was lower level of PIN1 expression in non-cancerous tissues; (2) 58.6% (17/29) HCC tissues showed beta-catenin protein accumulation in cytoplasm and nucleus. 46.2% (6/13) HCC tissues indicated beta-catenin protein accumulation with higher level of PIN1 expression, while 53.8% (7/13) HCC tissues indicated beta-catenin protein accumulation with lower level or trace of PIN1 expression (chi2=0.00, P>0.05); (3) 24.1% (7/29) of primary tumor lesions carried gene mutations in exon 3 of beta-catenin, and accompanied by beta-catenin protein accumulation. There was no mutation in non-cancerous tissues. All the mutation presented in tissues with low level of PIN1 expression. There was no mutation of beta-catenin gene in tissues with high PIN1 expression level (chi2=58.12, P<0.05). So it was postulated that the increase of PIN1 gene expression could promote hepatocellular carcinogenesis via a way different from beta-catenin gene mutation.
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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 |
Feb
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| pubmed:issn |
1672-0733
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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 |
54-7
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| pubmed:meshHeading |
pubmed-meshheading:17393110-Adult,
pubmed-meshheading:17393110-Aged,
pubmed-meshheading:17393110-Carcinoma, Hepatocellular,
pubmed-meshheading:17393110-Cell Nucleus,
pubmed-meshheading:17393110-Cytoplasm,
pubmed-meshheading:17393110-DNA, Neoplasm,
pubmed-meshheading:17393110-Female,
pubmed-meshheading:17393110-Humans,
pubmed-meshheading:17393110-Immunohistochemistry,
pubmed-meshheading:17393110-Liver Neoplasms,
pubmed-meshheading:17393110-Male,
pubmed-meshheading:17393110-Middle Aged,
pubmed-meshheading:17393110-Mutation,
pubmed-meshheading:17393110-Peptidylprolyl Isomerase,
pubmed-meshheading:17393110-Polymerase Chain Reaction,
pubmed-meshheading:17393110-Polymorphism, Single-Stranded Conformational,
pubmed-meshheading:17393110-Sequence Analysis, DNA,
pubmed-meshheading:17393110-beta Catenin
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| pubmed:year |
2007
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| pubmed:articleTitle |
PIN1 gene overexpression and beta-catenin gene mutation/expression in hepatocellular carcinoma and their significance.
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| pubmed:affiliation |
Department of Medical Genetics, School of Medical Sciences, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. huiwang1977@yahoo.com.cn
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| pubmed:publicationType |
Journal Article
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