Lian Zhaorui, Liu Jie, Li Li, Li Xianxing, Tufan N Lale Satiroglu, Clayton Marcy, Wu Meng-Chao, Wang Hong-Yang, Arbuthnot Patrick, Kew Michael, Feitelson Mark A
Department of Pathology, Anatomy, and Cell Biology, Thomas Jefferson University, Philadelphia, PA 19107, USA.
Neoplasia. 2003 May-Jun;5(3):229-44. doi: 10.1016/S1476-5586(03)80055-6.
Hepatitis B x antigen (HB x Ag) is a trans-activating protein that may be involved in hepatocarcinogenesis, although few natural effectors of HB x Ag that participate in this process have been identified. To identify additional effectors, whole cell RNA isolated from HB x Ag-positive and HB x Ag-negative HepG2 cells were compared by polymerase chain reaction select cDNA subtraction, and one clone, upregulated gene, clone 11 (URG11), was chosen for further characterization. Elevated levels of URG11 mRNA and protein were observed in HB x Ag-positive compared to HB x Ag-negative HepG2 cells. Costaining was observed in infected liver (P < 0.01). URG11 stimulated cell growth in culture (P < 0.01), anchorage-independent growth in soft agar (P < 0.001), and accelerated tumor formation (P < 0.01), and yielded larger tumors (P < 0.02) in SCID mice injected subcutaneously with HepG2 cells. These data suggest that URG11 is a natural effector of HB x Ag that may promote the development of hepatocellular carcinoma.
乙型肝炎X抗原（HBxAg）是一种反式激活蛋白，可能参与肝癌发生，尽管参与此过程的HBxAg天然效应分子鲜有被鉴定出来。为了鉴定其他效应分子，通过聚合酶链反应选择cDNA消减技术比较了从HBxAg阳性和HBxAg阴性的HepG2细胞中分离出的全细胞RNA，选择了一个克隆，上调基因克隆11（URG11）进行进一步表征。与HBxAg阴性的HepG2细胞相比，在HBxAg阳性的细胞中观察到URG11 mRNA和蛋白质水平升高。在受感染的肝脏中观察到共染色（P<0.01）。URG11在培养中刺激细胞生长（P<0.01），在软琼脂中刺激非贴壁依赖性生长（P<0.001），并加速肿瘤形成（P<0.01），在皮下注射HepG2细胞的SCID小鼠中产生更大的肿瘤（P<0.02）。这些数据表明，URG11是HBxAg的一种天然效应分子，可能促进肝细胞癌的发展。
