个人信息Personal Information
教授
博士生导师
硕士生导师
性别:男
毕业院校:日本京都大学
学位:博士
所在单位:化工海洋与生命学院
电子邮箱:jnzhang@dlut.edu.cn
Heparanase-1-induced shedding of heparan sulfate from syndecan-1 in hepatocarcinoma cell facilitates lymphatic endothelial cell proliferation via VEGF-C/ERK pathway
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论文类型:期刊论文
发表时间:2017-04-01
发表刊物:BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
收录刊物:SCIE、PubMed
卷号:485
期号:2
页面范围:432-439
ISSN号:0006-291X
关键字:Heparanase-1; Syndecan-1; Heparan sulfate; VEGF-C
摘要:Heparanase-1/syndecan-1 axis plays critical roles in tumorigenesis and development. The main mechanism includes heparanase-1 (HPA-1) degrades the heparan sulfate chain of syndecan-1 (SDC-1), and the following shedding of heparan sulfate from tumor cell releases and activates SDC-1 sequestered growth factors. However, the significance of Heparanase-1/syndecan-1 axis and its effects on the microenvironment of lymphatic metastasis in hepatocellular carcinogenesis (HCC) procession have not been reported. Herein, we found that IPA-1 could degrade the heparan sulfate on hepatocarcinoma cell surface. Importantly, HPA-1-induced shedding of heparan sulfate chain from SDC-1 facilitated the release of vascular endothelial growth factor C (VEGF-C) from SDC-1/VEGF-C complex into the medium of hepatocarcinoma cell. Further studies indicated that VEGF-C secretion from hepatocarcinoma cell promoted lymphatic endothelial cell growth through activating extracellular signal-regulated kinase (ERIC) signaling. Taken together, this study reveals a novel existence of Heparanase-1/syndecan-1 axis in hepatocarcinoma cell and its roles in the cross-talking with the microenvironment of lymphatic metastasis. (C) 2017 Elsevier Inc. All rights reserved.