Seifer M, Gerlich W H
Department of Medical Microbiology, University of Göttingen, Federal Republic of Germany.
Arch Virol. 1992;126(1-4):119-28. doi: 10.1007/BF01309689.
Previously we have shown that a nontumorigenic mouse hepatocyte line harboring simian virus 40 large tumor antigen (SV 40 TAg) could be converted to a full-malignant phenotype by transfection with HBV DNA. Using a permanent SV 40 TAg-negative mouse fibroblast cell line (LTK-), we studied whether the in vitro-oncogenicity of HBV was dependent on simultaneous expression of SV 40 TAg or not. Three fibroblast lines stably transfected by full-length HBV DNA formed four times more colonies of large size in soft agar than nontransfected LTK- cells. All three clones expressed high levels of HBx protein, but variable levels of other HBV proteins. A second type of clone that was transfected by a partial HBV genome and that expressed HBV surface but no HBx proteins, did not acquire increased growth in soft agar. These data reveal that HBV DNA can enhance malignant growth independent of SV 40 TAg and suggest that HBx protein may act as an HBV oncogene at least in vitro.
先前我们已经表明，携带猿猴病毒40大T抗原（SV 40 TAg）的非致瘤性小鼠肝细胞系通过转染乙肝病毒（HBV）DNA可转变为完全恶性表型。利用一种永久性的SV 40 TAg阴性小鼠成纤维细胞系（LTK-），我们研究了HBV的体外致癌性是否依赖于SV 40 TAg的同时表达。三个用全长HBV DNA稳定转染的成纤维细胞系在软琼脂中形成的大尺寸集落比未转染的LTK-细胞多四倍。所有三个克隆均高水平表达HBx蛋白，但其他HBV蛋白的表达水平各不相同。第二种类型的克隆用部分HBV基因组转染，表达HBV表面抗原但不表达HBx蛋白，在软琼脂中未获得生长增加。这些数据表明，HBV DNA可独立于SV 40 TAg增强恶性生长，并提示HBx蛋白至少在体外可能作为一种HBV癌基因发挥作用。
