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目的： 探讨间隙连接基因 ｃｘ３２，ｃｘ４３ 与肝细胞癌（ Ｈ Ｃ Ｃ） 发生的关系和作用机制． 方法： 应用 Ｓ Ｐ 免疫组织化学法和原位杂交技术，研究 Ｈ Ｃ Ｃ ６１ 例和正常肝组织１４ 例中ｃｘ３２，ｃｘ４３ 基因的表达规律． 结果： Ｃｘ３２ 蛋白在 Ｈ Ｃ Ｃ Ⅰ，Ⅱ，Ⅲ 级和正常肝中的阳性率分别为 ５５．６ ％ ， ４２．１％ ，１８．２％和 ９２．９％ ； Ｃｘ４３ 蛋白的阳性率分别为 ４４．４％ ， ２６． ３％ ，１２１％ 和 ７８．６％ ． Ｃｘ３２， Ｃｘ４３ 在 Ｈ Ｃ Ｃ各级和正常肝组织中存在显著性差异 （ Ｐ＜ ０．０５）． 原位杂交结果显示， Ｈ Ｃ Ｃ和正常肝中 ｃｘ３２，ｃｘ４３ ｍ Ｒ Ｎ Ａ 均保持较高水平，ｃｘ３２ ｍ Ｒ Ｎ Ａ 在 Ｈ Ｃ Ｃ Ⅰ，Ⅱ，Ⅲ 级和正常肝组织中的阳性率分别为 ８８．９％ ，８４．２％ ，８７．９％ 和 ９２９％ ；ｃｘ４３ ｍ Ｒ Ｎ Ａ 为 ７７．８％ ，７８．６％ ，７８８％ 和８５．７％ ， ｃｘ３２ 与ｃｘ４３ 基因在 Ｈ Ｃ Ｃ各级和正常肝中无显著性差异． 结论： ｃｘ３２，ｃｘ４３ 基因在转录后、翻译水平的调控异常，是其蛋白表达降低，导致 Ｈ Ｃ Ｃ发生的重要分子机制．
Objective: To investigate the relationship and mechanism of gap junction gene cx32, cx43 and hepatocellular carcinoma (H C C). Methods: The expression of cx32 and cx43 genes in 61 cases of H C C and 14 cases of normal liver tissues were studied by SP immunohistochemistry and in situ hybridization. Results: The positive rates of Cx32 protein in H C C I, II, III and normal liver were 55.6 %, 42.1%, 18.2% and 92.9% respectively; the positive rate of Cx43 protein was 44.4%, 26. 3%, 121% and 78.6%. Cx32, Cx43 were significantly different between H C C levels and normal liver tissues (P < 0.05). The results of in situ hybridization showed that the cx32 and cx43 m R N A levels in H C C and normal liver remained high, and the positive rates of cx32 m R N A in H C C I, II, III and normal liver tissues were respectively. It is 88.9%, 84.2%, 87.9% and 92.9%; cx43 m R N A is 77.8%, 78.6%, 78.8% and 85.7%, cx32 and cx43 Genes were not significantly different between H C C levels and normal liver. Conclusion: The abnormal regulation of cx32 and cx43 genes in post-transcriptional and translational levels is an important molecular mechanism for the reduction of protein expression and the occurrence of H C C.