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Updated: Jul 11, 2026

Visualizing Genetic Variants, Short Targets, and Point Mutations in the Morphological Tissue Context with an RNA In Situ Hybridization Assay
Published on: August 14, 2018
[Expression and exon 3 mutation of beta-catenin in human hepatocellular carcinoma]
Yang Jiao1, Ke-Chen Ban, Ji Cao
1Department of Pharmacology, Guangxi Medical University, Nanning, Guangxi, 530021, P. R. China.
Background & Objective:
South Guangxi is an area with high incidence of hepatocellular carcinoma (HCC), and with severe contamination of dietary aflatoxin B1 (AFB1). The activation of beta-Catenin is involved in many cancers. AFB1 may play a key role in hepatocarcinogenesis. This study was to explore the expression and mutation of beta-Catenin in HCC patients from the area with high exposure level of AFB1.
Methods:
The expression of beta-Catenin in 52 specimens of HCC and para-HCC tissues, and 18 specimens of non-cancerous liver tissues from South Guangxi were detected by direct sequencing, reverse transcription-polymerase chain reaction (RT-PCR), immunohistochemistry, and Western blot.
Results:
No mutation in exon 3 of beta-Catenin gene was found in HCC tissues. The mRNA level of beta-Catenin was significantly higher in HCC tissues than in para-HCC tissues and non-cancerous tissues (0.42+/-0.24 vs. 0.20+/-0.16 and 0.23+/-0.12, P<0.01). The positive rate of beta-Catenin was significantly higher in HCC tissues than in para-HCC tissues (55.8% vs. 36.5%, P<0.05). The expression of beta-Catenin mRNA showed no significant correlation to clinicopathologic parameters of HCC (all P>0.05), while the expression of beta-Catenin protein was significantly correlated to metastasis, relapse, portal vein embolus, and clinical stage (all P<0.05).
Conclusion:
Beta-catenin is overexpressed in HCC, but its overexpression has no correlation to gene mutation at GSK-3beta phosphorylation sites in exon 3.
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