Bae Si Hyun, Jung Eun Sun, Park Young Min, Jang Jeong Won, Choi Jong Young, Cho Se Hyun, Yoon Seung Kew, Ahn Byung Min, Cha Sang Bok, Chung Kyu Won, Sun Hee Sik, Park Doo Ho, Kim Byung Kee, Kim Dong Goo
Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul, Korea.
Taehan Kan Hakhoe Chi. 2002 Sep;8(3):297-303.
BACKGROUND/AIMS: E-cadherin is involved in intercellular binding and cellular polarity formation. beta-catenin plays a fundamental role in regulation of the E-cadherin cell adhesion complex. The abnormalities of the components of the complex may disrupt this adhesive function. We investigated the expression patterns of E-cadherin and beta-catenin to determine the clinical significance of these proteins in hepatocellular carcinoma.
MATERIALS/METHODS: Thirty-six hepaticellular carcinoma tissues and adjacent non-tumor specimens were analyzed. Subcellular distribution of E-cadherin and beta-catenin was examined by immunohistochemistry staining. We evaluated the patterns of the expression, and investigated the relationship with the cause of HCC; level of AFP; TNM stage; tumor size; growth types; metastasis; differentiation grade of HCC; and presence of portal vein thrombosis.
Immunohistochemistry showed that all non-tumor tissues had membranous type staining of E-cadherin. All non-tumor tissues showed cytoplasmic type staining of beta-catenin, but no beta-catenin accumulation in nuclei was found. 58% (21/36) of HCC showed positive expression of E-cadherin in cytoplasmic membrane. The cytoplasmic expression of beta-catenin in HCC was 83% (30/36); nuclear expression in 14% (5/36); and no staining in 3% (1/36). Nuclear beta-catenin expression was observed in none (0/4) of the well-differentiated HCC; 17%(3/9) of moderate-differentiated HCC; and 17%(2/6) of poorly-differentiated HCC. There were no relationships between E-cadherin and beta-catenin expression with other clinicopathologic factors.
Loss of cytoplasmic staining of E-cadherin and nuclear accumulation of beta-catenin were observed in HCC. Nuclear accumulation of beta-catenin was not found in well differentiated HCC but was found in poorly differentiated HCC.
背景/目的：E-钙黏蛋白参与细胞间黏附及细胞极性形成。β-连环蛋白在E-钙黏蛋白细胞黏附复合体的调控中起重要作用。该复合体成分异常可能会破坏这种黏附功能。我们研究了E-钙黏蛋白和β-连环蛋白的表达模式，以确定这些蛋白在肝细胞癌中的临床意义。
材料/方法：分析36例肝细胞癌组织及相邻非肿瘤标本。通过免疫组织化学染色检测E-钙黏蛋白和β-连环蛋白的亚细胞分布。我们评估了表达模式，并研究其与肝细胞癌病因、甲胎蛋白水平、TNM分期、肿瘤大小、生长类型、转移、肝细胞癌分化程度及门静脉血栓形成的关系。
免疫组织化学显示，所有非肿瘤组织E-钙黏蛋白呈膜型染色。所有非肿瘤组织β-连环蛋白呈胞质型染色，但未发现β-连环蛋白在细胞核内积聚。58%（21/36）的肝细胞癌E-钙黏蛋白在细胞质膜呈阳性表达。肝细胞癌中β-连环蛋白的胞质表达为83%（30/36）；核表达为14%（5/36）；无染色为3%（1/36）。在高分化肝细胞癌中未观察到核β-连环蛋白表达（0/4）；中分化肝细胞癌为17%（3/9）；低分化肝细胞癌为17%（2/6）。E-钙黏蛋白和β-连环蛋白表达与其他临床病理因素之间无相关性。
在肝细胞癌中观察到E-钙黏蛋白胞质染色缺失及β-连环蛋白核内积聚。高分化肝细胞癌未发现β-连环蛋白核内积聚，而低分化肝细胞癌中发现。
