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Topics {✒️}

peptidyl-proplyl-isomerase pin1 gene β-catenin gene mutation/expression month download article/chapter β-catenin protein accumulation β-catenin gene mutation b-catenin gene mutations beta-catenin activation β-catenin gene related subjects full article pdf human hepatocellular carcinoma pin1 regulates turnover t-cell factor-4 privacy choices/manage cookies pin1 gene overexpression pin1 gene expression β-catenin signaling prolyl isomerase pin1 promote hepatocellular carcinogenesis nat cell biol h-ras mutations correspondent abnormal expression hepatocellular carcinoma european economic area wnt proteins potential therapeutic target distinct oncogenic events conditions privacy policy check access instant access transductional pathways tongji medical college mouse hepatic carcinogenesis article wang accepting optional cookies article journal journal finder publish β-catenin article log pin1 gene beta-catenin nuclear accumulation mutation presented carcinoma tissues colon cancer cancer res article cite pin1 overexpression oncogenesis oncogene

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         headline:PIN1 gene overexpression and β-catenin gene mutation/expression in hepatocellular carcinoma and their significance
         description: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 β-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 β-catenin gene and differential expression of β-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 (x 2=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 β-catenin protein accumulation in cytoplasm and nucleus. 46.2% (6/13) HCC tissues indicated β-catenin protein accumulation with higher level of PIN1 expression, while 53.8% (7/13) HCC tissues indicated β-catenin protein accumulation with lower level or trace of PIN1 expression (x 2=0.00, P>0.05); (3) 24.1% (7/29) of primary tumor lesions carried gene mutations in exon 3 of β-catenin, and accompanied by β-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 β-catenin gene in tissues with high PIN1 expression level (x 2=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 β-catenin gene mutation.
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      headline:PIN1 gene overexpression and β-catenin gene mutation/expression in hepatocellular carcinoma and their significance
      description: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 β-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 β-catenin gene and differential expression of β-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 (x 2=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 β-catenin protein accumulation in cytoplasm and nucleus. 46.2% (6/13) HCC tissues indicated β-catenin protein accumulation with higher level of PIN1 expression, while 53.8% (7/13) HCC tissues indicated β-catenin protein accumulation with lower level or trace of PIN1 expression (x 2=0.00, P>0.05); (3) 24.1% (7/29) of primary tumor lesions carried gene mutations in exon 3 of β-catenin, and accompanied by β-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 β-catenin gene in tissues with high PIN1 expression level (x 2=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 β-catenin gene mutation.
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