北京大学医学部机构知识库
Advanced  
IR@PKUHSC  > 北京大学第二临床医学院  > 外科肿瘤研究室  > 期刊论文
学科主题: 临床医学
题名:
HSulf-1 inhibits cell proliferation and invasion in human gastric cancer
作者: Li, Jie1; Mo, Min-Li1; Chen, Zhao1; Yang, Jie1; Li, Qiu-Shi1; Wang, Dian-Jun2; Zhang, Hui3,4; Ye, Ying-Jiang3,4; Xu, Jun-Pu5; Li, Hai-Long6; Zhang, Fang6; Zhou, Hai-Meng1,6
刊名: CANCER SCIENCE
发表日期: 2011-10-01
DOI: 10.1111/j.1349-7006.2011.02024.x
卷: 102, 期:10, 页:1815-1821
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Oncology
研究领域[WOS]: Oncology
关键词[WOS]: HEPARAN-SULFATE PROTEOGLYCANS ; HEPATOCELLULAR-CARCINOMA ; SIGNALING PATHWAY ; TUMOR-GROWTH ; IN-VIVO ; WNT ; PROMOTES ; CATENIN ; GASTRULATION ; ANGIOGENESIS
英文摘要:

The HSulf-1 gene encodes an extracellular 6-O-endosulfatase and regulates the sulfation status of heparan sulfate proteoglycans (HSPG). We have demonstrated that promoter hypermethylation is correlated with the HSulf-1 silencing in gastric cancer. To investigate the functional importance of HSulf-1 silencing in gastric cancer, we restored HSulf-1 expression in the gastric cancer cell line MKN28, which lacks endogenous HSulf-1. Following restoration of expression, HSulf-1 inhibited cell proliferation, motility, and invasion in vitro, as well as significantly suppressing the MKN28 xenograft model (P < 0.05). No noticeable changes in proliferation and motility were observed following restoration of HSulf-1 in another gastric cancer cell line, namely AGS cells. Interestingly, in MKN28 cells, which have been reported to be dependent on extracellular Wnt signaling, we found that HSulf-1 inhibited the transcriptional activity of the Wnt/beta-catenin pathway and downregulated its targeted genes. Conversely, in AGS cells, in the constitutive Wnt/beta-catenin pathway is active, HSulf-1 had no effect on the activity of the Wnt/beta-catenin pathway. Furthermore, transfection of Wnt3a cDNA or beta-catenin shRNA resulted in rescue or enhancement, respectively, of the effects of HSulf-1 in MKN28 cells. Furthermore, HSPG epitope analysis confirmed that HSulf-1 affected the structure of heparan sulfate on the cell surface. Together, the results of the present study suggest that extracellular HSulf-1 may function as a negative regulator of proliferation and invasion in gastric cancer by suppressing Wnt/beta-catenin signaling at the cell surface. (Cancer Sci 2011; 102: 1815-1821)

语种: 英语
所属项目编号: 2007CB914401 ; 2011CB910803 ; 30770475
项目资助者: National Key Basic Research Project ; National Key Basic Research and Development (973) Program of China ; China Natural Science Foundation ; Beijing ACCB Biotech
WOS记录号: WOS:000304370600004
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/54375
Appears in Collections:北京大学第二临床医学院_外科肿瘤研究室_期刊论文

Files in This Item:

There are no files associated with this item.


作者单位: 1.Tsinghua Univ, Sch Life Sci, Beijing 100084, Peoples R China
2.Chinese Peoples Liberat Army Gen Hosp, Dept Pathol, Beijing, Peoples R China
3.Peking Univ Peoples Hosp, Surg Oncol Lab, Beijing, Peoples R China
4.Peking Univ Peoples Hosp, Dept Surg Gastroenterol, Beijing, Peoples R China
5.Beijing ACCB Biotech Ltd, Beijing, Peoples R China
6.Tsinghua Univ, Yangtze Delta Reg Inst, Zhejiang Prov Key Lab Appl Enzymol, Jiaxing, Zhejiang, Peoples R China

Recommended Citation:
Li, Jie,Mo, Min-Li,Chen, Zhao,et al. HSulf-1 inhibits cell proliferation and invasion in human gastric cancer[J]. CANCER SCIENCE,2011,102(10):1815-1821.
Service
Recommend this item
Sava as my favorate item
Show this item's statistics
Export Endnote File
Google Scholar
Similar articles in Google Scholar
[Li, Jie]'s Articles
[Mo, Min-Li]'s Articles
[Chen, Zhao]'s Articles
CSDL cross search
Similar articles in CSDL Cross Search
[Li, Jie]‘s Articles
[Mo, Min-Li]‘s Articles
[Chen, Zhao]‘s Articles
Related Copyright Policies
Null
Social Bookmarking
Add to CiteULike Add to Connotea Add to Del.icio.us Add to Digg Add to Reddit

Items in IR are protected by copyright, with all rights reserved, unless otherwise indicated.

 

 

Valid XHTML 1.0!
Copyright © 2007-2017  北京大学医学部 - Feedback
Powered by CSpace