Inhibitory Effect of Endostar on Specific Angiogenesis Induced by Human Hepatocellular Carcinoma

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 analysi...

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Main Authors: Qing Ye, Shukui Qin, Yanhong Liu, Jundong Feng, Qiong Wu, Wenshu Qu, Xiaojin Yin
Format: Article
Language:English
Published: Wiley 2015-01-01
Series:Gastroenterology Research and Practice
Online Access:http://dx.doi.org/10.1155/2015/957574
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author Qing Ye
Shukui Qin
Yanhong Liu
Jundong Feng
Qiong Wu
Wenshu Qu
Xiaojin Yin
author_facet Qing Ye
Shukui Qin
Yanhong Liu
Jundong Feng
Qiong Wu
Wenshu Qu
Xiaojin Yin
author_sort Qing Ye
collection DOAJ
description 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.
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spelling doaj-art-15b3a797534945e4ace755c50049bbeb2025-08-20T03:54:24ZengWileyGastroenterology Research and Practice1687-61211687-630X2015-01-01201510.1155/2015/957574957574Inhibitory Effect of Endostar on Specific Angiogenesis Induced by Human Hepatocellular CarcinomaQing Ye0Shukui Qin1Yanhong Liu2Jundong Feng3Qiong Wu4Wenshu Qu5Xiaojin Yin6Postdoctoral Station of Nanjing General Hospital, Nanjing 210002, ChinaPostdoctoral Station of Nanjing General Hospital, Nanjing 210002, ChinaDepartment of Pathology, Affiliated Drum Tower Hospital of Nanjing University Medical School, Nanjing 210008, ChinaPostdoctoral Station of Nanjing General Hospital, Nanjing 210002, ChinaPLA Cancer Center in Eighty-One Hospital of People's Liberation Army, Nanjing 210002, ChinaPLA Cancer Center in Eighty-One Hospital of People's Liberation Army, Nanjing 210002, ChinaJiangsu Harbinger Drug Development Co., Ltd., Nanjing 210002, ChinaTo 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.http://dx.doi.org/10.1155/2015/957574
spellingShingle Qing Ye
Shukui Qin
Yanhong Liu
Jundong Feng
Qiong Wu
Wenshu Qu
Xiaojin Yin
Inhibitory Effect of Endostar on Specific Angiogenesis Induced by Human Hepatocellular Carcinoma
Gastroenterology Research and Practice
title Inhibitory Effect of Endostar on Specific Angiogenesis Induced by Human Hepatocellular Carcinoma
title_full Inhibitory Effect of Endostar on Specific Angiogenesis Induced by Human Hepatocellular Carcinoma
title_fullStr Inhibitory Effect of Endostar on Specific Angiogenesis Induced by Human Hepatocellular Carcinoma
title_full_unstemmed Inhibitory Effect of Endostar on Specific Angiogenesis Induced by Human Hepatocellular Carcinoma
title_short Inhibitory Effect of Endostar on Specific Angiogenesis Induced by Human Hepatocellular Carcinoma
title_sort inhibitory effect of endostar on specific angiogenesis induced by human hepatocellular carcinoma
url http://dx.doi.org/10.1155/2015/957574
work_keys_str_mv AT qingye inhibitoryeffectofendostaronspecificangiogenesisinducedbyhumanhepatocellularcarcinoma
AT shukuiqin inhibitoryeffectofendostaronspecificangiogenesisinducedbyhumanhepatocellularcarcinoma
AT yanhongliu inhibitoryeffectofendostaronspecificangiogenesisinducedbyhumanhepatocellularcarcinoma
AT jundongfeng inhibitoryeffectofendostaronspecificangiogenesisinducedbyhumanhepatocellularcarcinoma
AT qiongwu inhibitoryeffectofendostaronspecificangiogenesisinducedbyhumanhepatocellularcarcinoma
AT wenshuqu inhibitoryeffectofendostaronspecificangiogenesisinducedbyhumanhepatocellularcarcinoma
AT xiaojinyin inhibitoryeffectofendostaronspecificangiogenesisinducedbyhumanhepatocellularcarcinoma