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Inhibition of Autocrine IGF-II on Effect of Human HepG2 Cell Proliferation and Angiogenesis Factor Expression

Inhibition of Autocrine IGF-II on Effect of Human HepG2 Cell Proliferation and Angiogenesis Factor Expression

Ninghua Yao, Dengfu Yao, Li Wang, Zhizhen Dong, Wei Wu, Liwei Qiu, Xiaodi Yan, Dandan Yu, Jie Chen, Wenli Sai, Haijian Zhang, Junlin Yang

Tumour Biol. 2012 Oct;33(5):1767-76.

PMID: 22684773

Abstract:

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.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
IAR42413311	IGF-II human			Price

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