Abstract

The aim of the present research was to investigate clinicopathologic correlations of immunohistochemically- demonstrated axin (axis inhibition) and β-catenin expression in primary hepatocellular carcinomas (HCCs), in comparison with paraneoplastic, cirrhotic and normal liver tissues. Variation in Axin expression across groups were significant (P < 0.01), correlating with alpha fetoprotein (AFP), HBsAg, cancer plugs in the portal vein, and clinical stage of HCCs(P < 0.05); however, there were no links with sex, age, and tumour size (P > 0.05). Differences in cell membrane β-catenin expression were also statistically significant (P < 0.01), again correlated with AFP, HBsAg, cancer plugs in the portal vein, and clinical stage in HCCs (P < 0.05) but not with sex, age, and tumour size (P > 0.05). Axin expression levels in tissues with reduced membrane β-catenin were low (P < 0.05), also being low with nuclear β-catenin expression (P < 0.05). Axin and β-catenin may play an important role in the genesis and progression of HCC via the Wnt signal transmission pathway. Simultaneous determination of axin, β-catenin, AFP, and HBsAg may be useful for early diagnosis, and metastatic and clinical staging of HCCs.

Highlights

  • The Wnt signal transduction pathway is composed of a series of cancer genes and tumour-suppressor genes that encodes proteins that contact each other and form a complex signal transmission network

  • Variation in Axin expression across groups were significant (P < 0.01), correlating with alpha fetoprotein (AFP), HBsAg, cancer plugs in the portal vein, and clinical stage of hepatocellular carcinomas (HCCs)(P < 0.05); there were no links with sex, age, and tumour size (P > 0.05)

  • The Wnt signal transduction pathway was discovered in the genetic analysis of fly polarity development and Xenopus laevis embryonic axiation, which plays an important regulatory role in cell proliferation, cell morphology, cell adhesion, cell movement, and body development and differentiation (Kikuchi et al, 1999)

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Summary

Introduction

The Wnt signal transduction pathway is composed of a series of cancer genes and tumour-suppressor genes that encodes proteins that contact each other and form a complex signal transmission network. Abnormalities in signal transduction are closely related to tumours and abnormal embryonic development (Kikuchi, 1999). Axin binds many important members of the Wnt signal transduction pathway, participates in many regulatory processes in signal transmission pathways, and plays a key role in individual development, cell proliferation, and carcinogenesis (Luo and Lin, 2004). Abnormal β-catenin expression mediates the abnormal activation of the Wnt signalling pathways, transforming membrane β-catenin into cytoplasmic and nuclear β-catenin; this increase in nuclear β-catenin levels activates target genes, initiates the cell cycle, and promotes cell hyperplasia, which eventually leads to tumour formation (Hasegawa et al, 2001)

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