Journal
MOLECULAR BIOLOGY REPORTS
Volume 39, Issue 5, Pages 5085-5093Publisher
SPRINGER
DOI: 10.1007/s11033-011-1304-2
Keywords
RNA interference; Vascular endothelial growth factor; Hepatocellular carcinoma; Migration; Proliferation
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Funding
- National natural Science Foundation of China [81170095, 30700306]
- Hubei Health Department Science Foundation [JX5B24]
- Hubei Education Department Science Foundation, China [T2008010, T201112, Q200524003]
- National Institutes of Health [HL093429, HL107526]
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Vascular endothelial growth factor (VEGF) plays a crucial role in tumor angiogenesis. VEGF induces new vessel formation and tumor growth by inducing mitogenesis and chemotaxis of normal endothelial cells and increasing vascular permeability. However, little is known about VEGF function in the proliferation, survival or migration of hepatocellular carcinoma cells (HCC). In the present study, we have found that VEGF receptors are expressed in HCC line BEL7402 and human HCC specimens. Importantly, VEGF receptor expression correlates with the development of the carcinoma. By using a comprehensive approaches including TUNEL assay, transwell and wound healing assays, migration and invasion assays, adhesion assay, western blot and quantitative RT-PCR, we have shown that knockdown of VEGF165 expression by shRNA inhibits the proliferation, migration, survival and adhesion ability of BEL7402. Knockdown of VEGF165 decreased the expression of NF-kappa B p65 and PKC alpha while increased the expression of p53 signaling molecules, suggesting that VEGF functions in HCC proliferation and migration are mediated by P65, PKC alpha and/or p53.
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