期刊
TUMOR BIOLOGY
卷 33, 期 5, 页码 1767-1776出版社
SAGE PUBLICATIONS LTD
DOI: 10.1007/s13277-012-0436-x
关键词
Hepatocellular carcinoma; Insulin-like growth factor II; Extrahepatic metastasis; Apoptosis; Targeted therapy
类别
资金
- Nantong Society Development [HS2011012]
- Jiangsu Health Projects [H2009025, K201102]
- Priority Academic Program Development and Scientific Innovating Plan of Jiangsu Education Institution, and the International S&T Cooperation Program of China [CXZZ11_0645]
Abnormal expression of insulin-like growth factor II (IGF-II) is associated with the hepatocyte malignant transformation and hepatocellular carcinoma (HCC) progress. In this study, specific IGF-II miRNA plasmids were constructed and transfected to HepG2 cells to knockdown IGF-II expression for observing effects on the cell proliferation, survival, apoptosis, angiogenesis, and anchorage-independent colony formation. IGF-II mRNA was evaluated by quantitative real-time polymerase chain reaction, and the level of IGF-II or vascular endothelial growth factor (VEGF) was quantitatively analyzed by ELISA. Our data shown that downregulation of IGF-II expression resulted in the viability alteration, proliferation inhibition, and apoptosis occurrence of HepG2 cells. The level of VEGF expression in the supernatant of HepG2 cells in the IGF-II-miRNA-transfected group was significantly decreasing (P < 0.01) than those in the untransfected group or the miRNA-neg-transfected group, with the susceptibility to anoikis and decreasing of anchorage-independent colony formation of HepG2 cells. Thus, we conclude that IGF-II is a potential molecular target for HCC gene therapy.
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