Little expression of proto-oncogene Bcl-2 in tumourous cells of hepatocellular carcinoma with chronic hepatitis C virus infection

Yoshiki Ito , Norio Hayashi , Yutaka Sasaki , Masayoshi Horimoto , Shigeo Wada , Yuji Tanaka , Taizo Hijioka , Kunio Suzuki , Hideyuki Fusamoto , Jiro Fujimoto , Eizo Okamoto , Takenobu Kamada
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引用次数: 4

Abstract

The proto-oncogene bcl-2, which was first found overexpressed in human follicular lymphoma, is now considered to inhibit apoptotic cell death, resulting in greater cell susceptibility to genetic alteration. Thus, this gene might cause hyperplasia or occasionally lead to a more malignant phase, i.e. carcinoma. Overexpression of this gene has been reported in several tumors. However, little has been clarified about its contribution to hepatocarcinogenesis. In this study, using immunoblotting, immunohistochemical and in situ hybridization techniques, we examined the expression of the bcl-2 protein and messenger RNA in patients having hepatocellular carcinoma with chronic hepatitis C virus infection. Immunoblot analysis indicated no significant differences in the amounts of bcl-2 protein between tumorous and nontumorous lesions. Furthermore, immunohistochemistry as well as in situ hybridization technique demonstrated that only lymphocytes infiltrating the tissues and tumors were bcl-2 positive. These findings suggest that the proto-oncogene bcl-2 may make no or little contribution, if any, to hepatocarcinogenesis.

原癌基因Bcl-2在慢性丙型肝炎病毒感染的肝癌肿瘤细胞中表达少
最初在人类滤泡性淋巴瘤中发现过表达的原癌基因bcl-2,现在被认为抑制凋亡细胞死亡,导致细胞对遗传改变的更大易感性。因此,该基因可能导致增生或偶尔导致更恶性的阶段,即癌。该基因的过表达已在几种肿瘤中被报道。然而,其在肝癌发生中的作用尚不清楚。在这项研究中,我们使用免疫印迹、免疫组织化学和原位杂交技术,检测了bcl-2蛋白和信使RNA在肝细胞癌合并慢性丙型肝炎病毒感染患者中的表达。免疫印迹分析显示肿瘤和非肿瘤病变中bcl-2蛋白的含量无显著差异。此外,免疫组织化学和原位杂交技术表明,只有浸润组织和肿瘤的淋巴细胞呈bcl-2阳性。这些发现表明原癌基因bcl-2可能对肝癌的发生没有贡献或贡献很小,如果有的话。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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