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Updated: Apr 12, 2026
Rat Mesentery Angiogenesis Assay
Published on: June 18, 2011
Inhibitory effect of endostar on specific angiogenesis induced by human hepatocellular carcinoma
Qing Ye1, Shukui Qin2, Yanhong Liu3
1Postdoctoral Station of Nanjing General Hospital, Nanjing 210002, China ; PLA Cancer Center in Eighty-One Hospital of People's Liberation Army, Nanjing 210002, China ; Department of Pathology, Affiliated Drum Tower Hospital of Nanjing University Medical School, Nanjing 210008, China.
Abstract:
To investigate the effect of endostar on specific angiogenesis induced by human hepatocellular carcinoma, this research systematically elucidated the inhibitory effect on HepG2-induced angiogenesis by endostar from 50 ng/mL to 50000 ng/mL. We employed fluorescence quantitative Boyden chamber analysis, wound-healing assay, flow cytometry examination using a coculture system, quantitative analysis of tube formation, and in vivo Matrigel plug assay induced by HCC conditioned media (HCM) and HepG2 compared with normal hepatocyte conditioned media (NCM) and L02. Then, we found that endostar as a tumor angiogenesis inhibitor could potently inhibit human umbilical vein endothelial cell (HUVEC) migration in response to HCM after four- to six-hour action, inhibit HCM-induced HUVEC migration to the lesion part in a dose-dependent manner between 50 ng/mL and 5000 ng/mL at 24 hours, and reduce HUVEC proliferation in a dose-dependent fashion. Endostar inhibited HepG2-induced tube formation of HUVECs which peaked at 50 ng/mL. In vivo Matrigel plug formation was also significantly reduced by endostar in HepG2 inducing system rather than in L02 inducing system. It could be concluded that, at cell level, endostar inhibited the angiogenesis-related biological behaviors of HUVEC in response to HCC, including migration, adhesion proliferation, and tube formation. At animal level, endostar inhibited the angiogenesis in response to HCC in Matrigel matrix.
Insights
Endostar effectively inhibits tumor angiogenesis in hepatocellular carcinoma (HCC) by reducing human umbilical vein endothelial cell migration, proliferation, and tube formation. This anti-angiogenic effect was observed both in vitro and in vivo.
Area of Science:
- Oncology
- Angiogenesis Research
- Biomedical Engineering
Background:
- Hepatocellular carcinoma (HCC) relies on angiogenesis for tumor growth and metastasis.
- Targeting tumor-specific angiogenesis is a key strategy in cancer therapy.
- Endostar, a recombinant human endostatin, has shown anti-angiogenic properties.
Purpose of the Study:
- To investigate the inhibitory effect of endostar on HCC-induced angiogenesis.
- To evaluate endostar's impact on human umbilical vein endothelial cell (HUVEC) behaviors in response to HCC.
- To assess endostar's efficacy in both in vitro and in vivo models of HCC angiogenesis.
Main Methods:
- Utilized fluorescence quantitative Boyden chamber analysis, wound-healing assays, and flow cytometry.
- Assessed HUVEC migration, proliferation, and tube formation in response to HCC conditioned media (HCM).
- Conducted in vivo Matrigel plug assays using HepG2-induced and L02-induced systems.
Main Results:
- Endostar potently inhibited HCM-induced HUVEC migration and proliferation in a dose-dependent manner.
- Endostar significantly reduced HepG2-induced HUVEC tube formation.
- In vivo, endostar markedly reduced Matrigel plug formation in the HepG2-induced system but not in the L02-induced system.
Conclusions:
- Endostar inhibits HCC-induced angiogenesis at the cellular level by impairing HUVEC migration, proliferation, and tube formation.
- Endostar demonstrates efficacy in reducing angiogenesis in vivo in response to HCC.
- Endostar represents a potential therapeutic agent for targeting angiogenesis in hepatocellular carcinoma.
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