School of Biological Science, Taishan Medical University, Chang Cheng Road, Taian 271016, People's Republic of China.
Mol Cell Biochem. 2012 May;364(1-2):165-71. doi: 10.1007/s11010-011-1215-5. Epub 2011 Dec 31.
Hepatocellular carcinoma (HCC) is a common malignancy and a leading cause of cancer death worldwide. Hepatitis B x-interacting protein (HBXIP), a cofactor of survivin, was originally identified by binding with the C-terminus of the HBx and negatively regulated the activity of HBx. In this study, the effect of HBXIP on the hepatoma cells-induced angiogenesis was investigated. Proliferation and migration of human umbilical vein endothelial cells (HUVECs) were detected by MTT and transwell assay, respectively. Tube formation and chick chorioallantoic membrane model were used to observe the angiogenesis. Vascular endothelial growth factor activity was assayed using ELISA kits. Western blotting was performed to examine the protein expression. Our results indicated that overexpression of HBXIP increased HepG2 cell-induced endothelial cells migration, proliferation, and angiogenesis, which may be related to increasing phosphorylation of endothelial NO synthase in HUVECs. These results suggest that HBXIP may play an important role in tumorigenesis by enhancing angiogenesis in HCC.
肝细胞癌（HCC）是一种常见的恶性肿瘤，也是全球癌症死亡的主要原因。乙型肝炎病毒 X 相互作用蛋白（HBXIP）是存活素的辅助因子，最初通过与 HBx 的 C 末端结合被鉴定出来，并负调控 HBx 的活性。在这项研究中，研究了 HBXIP 对肝癌细胞诱导的血管生成的影响。通过 MTT 和 Transwell 分析分别检测人脐静脉内皮细胞（HUVEC）的增殖和迁移。管形成和鸡胚尿囊膜模型用于观察血管生成。使用 ELISA 试剂盒测定血管内皮生长因子活性。通过 Western blot 检测蛋白表达。我们的结果表明，HBXIP 的过表达增加了 HepG2 细胞诱导的内皮细胞迁移、增殖和血管生成，这可能与 HUVECs 中内皮型一氧化氮合酶的磷酸化增加有关。这些结果表明，HBXIP 通过增强 HCC 中的血管生成可能在肿瘤发生中发挥重要作用。
