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Focal adhesion kinase is overexpressed in hepatocellular carcinoma and can be served as an independent prognostic factor
The development of human malignancies can be attributed to aberrant regulation of intracellular signal transduction pathways. In the current study, we aimed to evaluate focal adhesion kinase (FAK), a non-receptor tyrosine kinase, expression in hepatocellular carcinoma (HCC), and to explore the progn...
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Published in: | Journal of hepatology 2004-07, Vol.41 (1), p.104-111 |
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Main Authors: | , , , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | The development of human malignancies can be attributed to aberrant regulation of intracellular signal transduction pathways. In the current study, we aimed to evaluate focal adhesion kinase (FAK), a non-receptor tyrosine kinase, expression in hepatocellular carcinoma (HCC), and to explore the prognostic significance of FAK.
We investigated FAK mRNA expression in 60 HCC specimens using quantitative real-time reverse transcription polymerase chain reaction analysis, and the correlation between FAK expression and clinicopathologic parameters. FAK protein expression was examined using Western blot analysis and an immunohistochemical study.
We found that FAK mRNA was overexpressed in HCCs compared with the corresponding non-cancerous liver tissues (
P=0.0008). The FAK overexpression correlated significantly with tumor size (
P=0.034) and serum AFP level (
P=0.030). Univariate and multivariate analyses revealed that FAK mRNA expression was an independent prognostic factor for disease-free (risk ratio 3.83;
P=0.024) and overall (risk ratio 7.14;
P=0.015) survival. Besides, we confirmed immunohistochemically that the FAK protein was detectable in cancer cells despite non-expression in corresponding non-cancerous tissues.
Our results suggest that FAK mRNA expression has prognostic significance for the survival of patients with HCC. |
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ISSN: | 0168-8278 1600-0641 |
DOI: | 10.1016/j.jhep.2004.03.029 |