Original Articles
Copyright ©The Author(s) 2000. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Feb 15, 2000; 6(1): 66-69
Published online Feb 15, 2000. doi: 10.3748/wjg.v6.i1.66
Expression of gap junction genes connexin 32, connexin 43 and their proteins in hepatocellular carcinoma and normal liver tissues
Xiang-Dong Ma, Yan-Fang Sui, Wen-Liang Wang
Xiang-Dong Ma, Yan-Fang Sui, Wen-Liang Wang, Department of Pathology, the Fourth Military Medical University, 17 Changle Xilu, Xi’an 710033, Shaanxi Province, China
Xiang-Dong Ma, female, born on 1969-11-18 in Xi’an, Shaanxi Province, graduated from the Fourth Military Medical University as a doctor in 1999, now a lecturer, having 15 papers published.
Author contributions: All authors contributed equally to the work.
Correspondence to: Dr. Xiang-Dong Ma, Department of Obstetrics & Gynecology, Xijing Hospital, the Fourth Military Medical University, Xi’an 710033, Shaanxi Province, China. maping@FMMU.edu.cn
Received: June 23, 1999
Revised: September 2, 1999
Accepted: September 18, 1999
Published online: February 15, 2000
Abstract

AIM: To investigate the significance and mechanism of cx-32 mRNA, cx-43 mRNA and their proteins in hepatocarcinogenesis.

METHODS: Sixty-one cases of HCC and 14 cases of normal liver tissues were detected by immunohistochemical and in situ hybridization (ISH) methods.

RESULTS: In HCC grades I, II, III and normal liver tissues, the positive rates of Cx32 protein were 55.6%, 42.1%, 18.2% and 92.9%, respectively. The detection rates of Cx43 protein were 44%, 26.3%, 12.1% and 78.6%, respectively. There was significant difference in Cx32 and Cx43 protein between HCC and normal liver tissues (P < 0.01). ISH the positive rates of cx 32 mRNA shown by ISH in HCC grades I, II, III and normal liver tissues were 88.9%, 84.2%, 87.9% and 92.9%, respectively. Those of cx43 mRNA were 77.8%, 78.6%, 78. 8% and 85.7%, respectively. There was no statistical difference in the positive rates of cx32 mRNA and cx43 mRNA between HCC and normal liver tissue (P > 0.05).

CONCLUSION: The aberrant location of Cx32 and Cx43 proteins could be responsible for progression of hepatocarcinogenesis, and the defect of cx genes in post-translational processing might be the possible mechanism.

Keywords: connexin; gap junction; liver neoplasm; immunohistochemistry; in situ hybridization; carcinoma, hepatocellular; gene expression