Downregulation of NDRG1 promotes invasion of human gastric cancer AGS cells through MMP-2
The N-myc downstream-regulated gene-1 (NDRG1) has recently been proposed as a metastasis suppressor, but its precise role remains unclear. To investigate whether NDRG1 can indeed influence the metastasis progress, expression of endogenous NDRG1 was knocked down in human AGS gastric adenocarcinoma ce...
Gespeichert in:
Veröffentlicht in: | Tumor biology 2011-02, Vol.32 (1), p.99-105 |
---|---|
Hauptverfasser: | , , , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
container_end_page | 105 |
---|---|
container_issue | 1 |
container_start_page | 99 |
container_title | Tumor biology |
container_volume | 32 |
creator | Liu, Yan-li Bai, Wen-tao Luo, Wen Zhang, De-xin Yan, Yan Xu, Zhi-kai Zhang, Fang-lin |
description | The N-myc downstream-regulated gene-1 (NDRG1) has recently been proposed as a metastasis suppressor, but its precise role remains unclear. To investigate whether NDRG1 can indeed influence the metastasis progress, expression of endogenous NDRG1 was knocked down in human AGS gastric adenocarcinoma cells using RNA interference. Stable NDRG1 “silenced” transfectants showed similar growth rates as their control counterparts. By contrast, invasive ability in Matrigel invasion activity and Gelatinolytic activity by matrix metalloproteinase-2 (MMP-2) were markedly increased in NDRG1 “silenced” cells. Moreover, re-expression of NDRG1 by recombinant adenovirus Ad-NDRG1 in NDRG1 “silenced” cells inhibited the increased invasive ability. Further study, we found the induction of MMP-2 by downregulation of NDRG1 was mediated by MT1-MMP. Altogether, our results imply that NDRG-1 could play a key role in the regulation of cellular invasion and metastasis, which may involve the upregulation of matrix metalloproteinases. |
doi_str_mv | 10.1007/s13277-010-0103-z |
format | Article |
fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_818645183</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2248827121</sourcerecordid><originalsourceid>FETCH-LOGICAL-c370t-998ee21c533b989eeb752581335aefdaaaf1a3cab9d63976ecf6b13e7f7d4ccf3</originalsourceid><addsrcrecordid>eNp1kEtP3DAUha0KVB7tD-gGWWy6Cvj6JrG9RFAGJB5VH4uuLMdzMxM0icFOQPDrSTTTVkJicWVL57vnHh3GvoA4AiHUcQKUSmUCxDSYvXxgu5BLzARqsTX-JyWXGnfYXkp3QkBhTPmR7UgQhdQGdtmfs_DURVoMK9c3oeOh5jdnP2bA72NoQ0-JN92jSxtpObSu4wuX-th47l3nKfKT2U_uabVKvF_GMCyW_Pr6eyY_se3arRJ93rz77Pf5t1-nF9nV7ezy9OQq86hEnxmjiST4ArEy2hBVqpCFBsTCUT13ztXg0LvKzEs0qiRflxUgqVrNc-9r3Gdf175j4oeBUm_bJk15XEdhSFaDLvMCNI7k4RvyLgyxG8NZnSvMdS4mCNaQjyGlSLW9j03r4rMFYafW7bp1O3Y7DdqXcedgYzxULc3_bfyteQTkGkij1C0o_r_8vusrA1KM5A</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>847348403</pqid></control><display><type>article</type><title>Downregulation of NDRG1 promotes invasion of human gastric cancer AGS cells through MMP-2</title><source>MEDLINE</source><source>Springer Nature - Complete Springer Journals</source><creator>Liu, Yan-li ; Bai, Wen-tao ; Luo, Wen ; Zhang, De-xin ; Yan, Yan ; Xu, Zhi-kai ; Zhang, Fang-lin</creator><creatorcontrib>Liu, Yan-li ; Bai, Wen-tao ; Luo, Wen ; Zhang, De-xin ; Yan, Yan ; Xu, Zhi-kai ; Zhang, Fang-lin</creatorcontrib><description>The N-myc downstream-regulated gene-1 (NDRG1) has recently been proposed as a metastasis suppressor, but its precise role remains unclear. To investigate whether NDRG1 can indeed influence the metastasis progress, expression of endogenous NDRG1 was knocked down in human AGS gastric adenocarcinoma cells using RNA interference. Stable NDRG1 “silenced” transfectants showed similar growth rates as their control counterparts. By contrast, invasive ability in Matrigel invasion activity and Gelatinolytic activity by matrix metalloproteinase-2 (MMP-2) were markedly increased in NDRG1 “silenced” cells. Moreover, re-expression of NDRG1 by recombinant adenovirus Ad-NDRG1 in NDRG1 “silenced” cells inhibited the increased invasive ability. Further study, we found the induction of MMP-2 by downregulation of NDRG1 was mediated by MT1-MMP. Altogether, our results imply that NDRG-1 could play a key role in the regulation of cellular invasion and metastasis, which may involve the upregulation of matrix metalloproteinases.</description><identifier>ISSN: 1010-4283</identifier><identifier>EISSN: 1423-0380</identifier><identifier>DOI: 10.1007/s13277-010-0103-z</identifier><identifier>PMID: 21052891</identifier><language>eng</language><publisher>Dordrecht: Springer Netherlands</publisher><subject>Adenocarcinoma - enzymology ; Adenocarcinoma - pathology ; Biomedical and Life Sciences ; Biomedicine ; Blotting, Western ; Cancer ; Cancer Research ; Cell adhesion & migration ; Cell Cycle Proteins - antagonists & inhibitors ; Cell Cycle Proteins - genetics ; Cell Cycle Proteins - metabolism ; Cell Line, Tumor ; Down-Regulation ; Gastrointestinal diseases ; Gene expression ; Gene Expression Regulation, Neoplastic - physiology ; Humans ; Intracellular Signaling Peptides and Proteins - antagonists & inhibitors ; Intracellular Signaling Peptides and Proteins - genetics ; Intracellular Signaling Peptides and Proteins - metabolism ; Matrix Metalloproteinase 14 - metabolism ; Matrix Metalloproteinase 2 - metabolism ; Metastasis ; Neoplasm Invasiveness ; Proteins ; Research Article ; RNA, Small Interfering - genetics ; Stomach Neoplasms - enzymology ; Stomach Neoplasms - pathology</subject><ispartof>Tumor biology, 2011-02, Vol.32 (1), p.99-105</ispartof><rights>International Society of Oncology and BioMarkers (ISOBM) 2010</rights><rights>International Society of Oncology and BioMarkers (ISOBM) 2011</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c370t-998ee21c533b989eeb752581335aefdaaaf1a3cab9d63976ecf6b13e7f7d4ccf3</citedby><cites>FETCH-LOGICAL-c370t-998ee21c533b989eeb752581335aefdaaaf1a3cab9d63976ecf6b13e7f7d4ccf3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s13277-010-0103-z$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s13277-010-0103-z$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21052891$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Yan-li</creatorcontrib><creatorcontrib>Bai, Wen-tao</creatorcontrib><creatorcontrib>Luo, Wen</creatorcontrib><creatorcontrib>Zhang, De-xin</creatorcontrib><creatorcontrib>Yan, Yan</creatorcontrib><creatorcontrib>Xu, Zhi-kai</creatorcontrib><creatorcontrib>Zhang, Fang-lin</creatorcontrib><title>Downregulation of NDRG1 promotes invasion of human gastric cancer AGS cells through MMP-2</title><title>Tumor biology</title><addtitle>Tumor Biol</addtitle><addtitle>Tumour Biol</addtitle><description>The N-myc downstream-regulated gene-1 (NDRG1) has recently been proposed as a metastasis suppressor, but its precise role remains unclear. To investigate whether NDRG1 can indeed influence the metastasis progress, expression of endogenous NDRG1 was knocked down in human AGS gastric adenocarcinoma cells using RNA interference. Stable NDRG1 “silenced” transfectants showed similar growth rates as their control counterparts. By contrast, invasive ability in Matrigel invasion activity and Gelatinolytic activity by matrix metalloproteinase-2 (MMP-2) were markedly increased in NDRG1 “silenced” cells. Moreover, re-expression of NDRG1 by recombinant adenovirus Ad-NDRG1 in NDRG1 “silenced” cells inhibited the increased invasive ability. Further study, we found the induction of MMP-2 by downregulation of NDRG1 was mediated by MT1-MMP. Altogether, our results imply that NDRG-1 could play a key role in the regulation of cellular invasion and metastasis, which may involve the upregulation of matrix metalloproteinases.</description><subject>Adenocarcinoma - enzymology</subject><subject>Adenocarcinoma - pathology</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Blotting, Western</subject><subject>Cancer</subject><subject>Cancer Research</subject><subject>Cell adhesion & migration</subject><subject>Cell Cycle Proteins - antagonists & inhibitors</subject><subject>Cell Cycle Proteins - genetics</subject><subject>Cell Cycle Proteins - metabolism</subject><subject>Cell Line, Tumor</subject><subject>Down-Regulation</subject><subject>Gastrointestinal diseases</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic - physiology</subject><subject>Humans</subject><subject>Intracellular Signaling Peptides and Proteins - antagonists & inhibitors</subject><subject>Intracellular Signaling Peptides and Proteins - genetics</subject><subject>Intracellular Signaling Peptides and Proteins - metabolism</subject><subject>Matrix Metalloproteinase 14 - metabolism</subject><subject>Matrix Metalloproteinase 2 - metabolism</subject><subject>Metastasis</subject><subject>Neoplasm Invasiveness</subject><subject>Proteins</subject><subject>Research Article</subject><subject>RNA, Small Interfering - genetics</subject><subject>Stomach Neoplasms - enzymology</subject><subject>Stomach Neoplasms - pathology</subject><issn>1010-4283</issn><issn>1423-0380</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp1kEtP3DAUha0KVB7tD-gGWWy6Cvj6JrG9RFAGJB5VH4uuLMdzMxM0icFOQPDrSTTTVkJicWVL57vnHh3GvoA4AiHUcQKUSmUCxDSYvXxgu5BLzARqsTX-JyWXGnfYXkp3QkBhTPmR7UgQhdQGdtmfs_DURVoMK9c3oeOh5jdnP2bA72NoQ0-JN92jSxtpObSu4wuX-th47l3nKfKT2U_uabVKvF_GMCyW_Pr6eyY_se3arRJ93rz77Pf5t1-nF9nV7ezy9OQq86hEnxmjiST4ArEy2hBVqpCFBsTCUT13ztXg0LvKzEs0qiRflxUgqVrNc-9r3Gdf175j4oeBUm_bJk15XEdhSFaDLvMCNI7k4RvyLgyxG8NZnSvMdS4mCNaQjyGlSLW9j03r4rMFYafW7bp1O3Y7DdqXcedgYzxULc3_bfyteQTkGkij1C0o_r_8vusrA1KM5A</recordid><startdate>20110201</startdate><enddate>20110201</enddate><creator>Liu, Yan-li</creator><creator>Bai, Wen-tao</creator><creator>Luo, Wen</creator><creator>Zhang, De-xin</creator><creator>Yan, Yan</creator><creator>Xu, Zhi-kai</creator><creator>Zhang, Fang-lin</creator><general>Springer Netherlands</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7T5</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20110201</creationdate><title>Downregulation of NDRG1 promotes invasion of human gastric cancer AGS cells through MMP-2</title><author>Liu, Yan-li ; Bai, Wen-tao ; Luo, Wen ; Zhang, De-xin ; Yan, Yan ; Xu, Zhi-kai ; Zhang, Fang-lin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c370t-998ee21c533b989eeb752581335aefdaaaf1a3cab9d63976ecf6b13e7f7d4ccf3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Adenocarcinoma - enzymology</topic><topic>Adenocarcinoma - pathology</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Blotting, Western</topic><topic>Cancer</topic><topic>Cancer Research</topic><topic>Cell adhesion & migration</topic><topic>Cell Cycle Proteins - antagonists & inhibitors</topic><topic>Cell Cycle Proteins - genetics</topic><topic>Cell Cycle Proteins - metabolism</topic><topic>Cell Line, Tumor</topic><topic>Down-Regulation</topic><topic>Gastrointestinal diseases</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Neoplastic - physiology</topic><topic>Humans</topic><topic>Intracellular Signaling Peptides and Proteins - antagonists & inhibitors</topic><topic>Intracellular Signaling Peptides and Proteins - genetics</topic><topic>Intracellular Signaling Peptides and Proteins - metabolism</topic><topic>Matrix Metalloproteinase 14 - metabolism</topic><topic>Matrix Metalloproteinase 2 - metabolism</topic><topic>Metastasis</topic><topic>Neoplasm Invasiveness</topic><topic>Proteins</topic><topic>Research Article</topic><topic>RNA, Small Interfering - genetics</topic><topic>Stomach Neoplasms - enzymology</topic><topic>Stomach Neoplasms - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Yan-li</creatorcontrib><creatorcontrib>Bai, Wen-tao</creatorcontrib><creatorcontrib>Luo, Wen</creatorcontrib><creatorcontrib>Zhang, De-xin</creatorcontrib><creatorcontrib>Yan, Yan</creatorcontrib><creatorcontrib>Xu, Zhi-kai</creatorcontrib><creatorcontrib>Zhang, Fang-lin</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Tumor biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Yan-li</au><au>Bai, Wen-tao</au><au>Luo, Wen</au><au>Zhang, De-xin</au><au>Yan, Yan</au><au>Xu, Zhi-kai</au><au>Zhang, Fang-lin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Downregulation of NDRG1 promotes invasion of human gastric cancer AGS cells through MMP-2</atitle><jtitle>Tumor biology</jtitle><stitle>Tumor Biol</stitle><addtitle>Tumour Biol</addtitle><date>2011-02-01</date><risdate>2011</risdate><volume>32</volume><issue>1</issue><spage>99</spage><epage>105</epage><pages>99-105</pages><issn>1010-4283</issn><eissn>1423-0380</eissn><abstract>The N-myc downstream-regulated gene-1 (NDRG1) has recently been proposed as a metastasis suppressor, but its precise role remains unclear. To investigate whether NDRG1 can indeed influence the metastasis progress, expression of endogenous NDRG1 was knocked down in human AGS gastric adenocarcinoma cells using RNA interference. Stable NDRG1 “silenced” transfectants showed similar growth rates as their control counterparts. By contrast, invasive ability in Matrigel invasion activity and Gelatinolytic activity by matrix metalloproteinase-2 (MMP-2) were markedly increased in NDRG1 “silenced” cells. Moreover, re-expression of NDRG1 by recombinant adenovirus Ad-NDRG1 in NDRG1 “silenced” cells inhibited the increased invasive ability. Further study, we found the induction of MMP-2 by downregulation of NDRG1 was mediated by MT1-MMP. Altogether, our results imply that NDRG-1 could play a key role in the regulation of cellular invasion and metastasis, which may involve the upregulation of matrix metalloproteinases.</abstract><cop>Dordrecht</cop><pub>Springer Netherlands</pub><pmid>21052891</pmid><doi>10.1007/s13277-010-0103-z</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
fulltext | fulltext |
identifier | ISSN: 1010-4283 |
ispartof | Tumor biology, 2011-02, Vol.32 (1), p.99-105 |
issn | 1010-4283 1423-0380 |
language | eng |
recordid | cdi_proquest_miscellaneous_818645183 |
source | MEDLINE; Springer Nature - Complete Springer Journals |
subjects | Adenocarcinoma - enzymology Adenocarcinoma - pathology Biomedical and Life Sciences Biomedicine Blotting, Western Cancer Cancer Research Cell adhesion & migration Cell Cycle Proteins - antagonists & inhibitors Cell Cycle Proteins - genetics Cell Cycle Proteins - metabolism Cell Line, Tumor Down-Regulation Gastrointestinal diseases Gene expression Gene Expression Regulation, Neoplastic - physiology Humans Intracellular Signaling Peptides and Proteins - antagonists & inhibitors Intracellular Signaling Peptides and Proteins - genetics Intracellular Signaling Peptides and Proteins - metabolism Matrix Metalloproteinase 14 - metabolism Matrix Metalloproteinase 2 - metabolism Metastasis Neoplasm Invasiveness Proteins Research Article RNA, Small Interfering - genetics Stomach Neoplasms - enzymology Stomach Neoplasms - pathology |
title | Downregulation of NDRG1 promotes invasion of human gastric cancer AGS cells through MMP-2 |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-12T15%3A59%3A51IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Downregulation%20of%20NDRG1%20promotes%20invasion%20of%20human%20gastric%20cancer%20AGS%20cells%20through%20MMP-2&rft.jtitle=Tumor%20biology&rft.au=Liu,%20Yan-li&rft.date=2011-02-01&rft.volume=32&rft.issue=1&rft.spage=99&rft.epage=105&rft.pages=99-105&rft.issn=1010-4283&rft.eissn=1423-0380&rft_id=info:doi/10.1007/s13277-010-0103-z&rft_dat=%3Cproquest_cross%3E2248827121%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=847348403&rft_id=info:pmid/21052891&rfr_iscdi=true |