Ray R B, Lagging L M, Meyer K, Steele R, Ray R
Division of Infectious Disease and Immunology, Saint Louis University Health Sciences Center, MO 63110-0250, USA.
Virus Res. 1995 Aug;37(3):209-20. doi: 10.1016/0168-1702(95)00034-n.
The genomic region encoding the hepatitis C virus (HCV) core protein was cloned into a mammalian expression vector to study its role on the transcriptional regulation of cellular proto-oncogene and viral promoters. Using a transient transfection assay in human hepatocellular carcinoma (HepG2) cells, we demonstrate that the HCV core protein activates the human c-myc, Rous sarcoma virus long terminal repeat (LTR), and simian virus 40 (SV40) early promoters; and suppresses the c-fos promoter and human immunodeficiency virus type 1 (HIV-1) LTR activity. The transcriptional regulation of cellular proto-oncogenes by the HCV core protein suggests possible involvement of the core protein in the deregulation of normal hepatocyte growth and hepatocarcinogenesis.
将编码丙型肝炎病毒（HCV）核心蛋白的基因组区域克隆到哺乳动物表达载体中，以研究其对细胞原癌基因和病毒启动子转录调控的作用。通过在人肝癌（HepG2）细胞中进行瞬时转染实验，我们证明HCV核心蛋白可激活人c-myc、劳氏肉瘤病毒长末端重复序列（LTR）和猿猴病毒40（SV40）早期启动子；并抑制c-fos启动子和人类免疫缺陷病毒1型（HIV-1）LTR活性。HCV核心蛋白对细胞原癌基因的转录调控提示核心蛋白可能参与正常肝细胞生长失调和肝癌发生过程。
