NS-398 promotes pancreatic cancer cell invasion by CD147 and MMP-2 via the activation of P38
The overexpression or abnormal activation of cyclo-oxygenase-2 (COX-2) has been reported in pancreatic cancer cells. NS-398, a selective inhibitor of COX-2, is unable to inhibit pancreatic cancer cell proliferation, as determined by a Cell Counting Kit 8 assay. However, it does increase cancer cell...
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| Veröffentlicht in: | Molecular medicine reports 2016-03, Vol.13 (3), p.2208-2214 |
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| creator | LIU, HUA XU, XUAN-FU ZHAO, YAN TANG, MAO-CHUN ZHOU, YING-QUN GAO, FENG-HOU |
| description | The overexpression or abnormal activation of cyclo-oxygenase-2 (COX-2) has been reported in pancreatic cancer cells. NS-398, a selective inhibitor of COX-2, is unable to inhibit pancreatic cancer cell proliferation, as determined by a Cell Counting Kit 8 assay. However, it does increase cancer cell invasiveness, and therefore the invasiveness of the PANC-1 cells was determined, along with the activation of P38, which was assessed by western blotting. In the present study, to evaluate the mechanisms underlying the action of NS-398 in pancreatic cancer cells, PANC-1 cells were treated with NS-398, and the invasion signaling pathways of cluster of differentiation (CD)147-matrix metalloproteinase (MMP)-2 and mitogen-activated protein kinases were evaluated. The results showed that NS-398-induced the expression of CD147 and MMP-2 via the activation of P38, which was involved in antiproliferative activity and induced pancreatic cancer cell invasiveness. The PANC-1 cells were also co-treated with CD147 small interfering (si)RNA and NS-398, and it was found that the NS-398-induced activation of P38 was not inhibited by CD147 siRNA, however, the expression of MMP-2 was inhibited. CD147 siRNA inhibited the invasiveness of the pancreatic cancer cells induced by NS-398, but also restored NS-398-induced antiproliferative activity. These data indicated that P38 in the pancreatic cancer cells was non-specifically activated by NS-398. This activation induced the expression of CD147-MMP-2, opposed the antiproliferative activity of NS-398 and increased the invasiveness of the PANC-1 cells. |
| doi_str_mv | 10.3892/mmr.2016.4783 |
| format | Article |
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NS-398, a selective inhibitor of COX-2, is unable to inhibit pancreatic cancer cell proliferation, as determined by a Cell Counting Kit 8 assay. However, it does increase cancer cell invasiveness, and therefore the invasiveness of the PANC-1 cells was determined, along with the activation of P38, which was assessed by western blotting. In the present study, to evaluate the mechanisms underlying the action of NS-398 in pancreatic cancer cells, PANC-1 cells were treated with NS-398, and the invasion signaling pathways of cluster of differentiation (CD)147-matrix metalloproteinase (MMP)-2 and mitogen-activated protein kinases were evaluated. The results showed that NS-398-induced the expression of CD147 and MMP-2 via the activation of P38, which was involved in antiproliferative activity and induced pancreatic cancer cell invasiveness. The PANC-1 cells were also co-treated with CD147 small interfering (si)RNA and NS-398, and it was found that the NS-398-induced activation of P38 was not inhibited by CD147 siRNA, however, the expression of MMP-2 was inhibited. CD147 siRNA inhibited the invasiveness of the pancreatic cancer cells induced by NS-398, but also restored NS-398-induced antiproliferative activity. These data indicated that P38 in the pancreatic cancer cells was non-specifically activated by NS-398. This activation induced the expression of CD147-MMP-2, opposed the antiproliferative activity of NS-398 and increased the invasiveness of the PANC-1 cells.</description><identifier>ISSN: 1791-2997</identifier><identifier>EISSN: 1791-3004</identifier><identifier>DOI: 10.3892/mmr.2016.4783</identifier><identifier>PMID: 26782265</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Basigin - metabolism ; Cadmium ; CD147 antigen ; Cell growth ; Cell Line, Tumor ; Cell proliferation ; Cell Proliferation - drug effects ; cluster of differentiation 147 ; Cyclooxygenase-2 ; Cyclooxygenases ; Development and progression ; Enzyme Activation - drug effects ; Enzymes ; Gelatinase A ; Gene expression ; Genetic aspects ; Health aspects ; Humans ; Imidazoles - pharmacology ; invasion ; Invasiveness ; Laboratories ; MAP Kinase Signaling System - drug effects ; Matrix metalloproteinase ; Matrix Metalloproteinase 2 - metabolism ; matrix metalloproteinase-2 ; Medical prognosis ; Metalloproteinase ; Metastasis ; Neoplasm Invasiveness ; Nitrobenzenes - pharmacology ; Nitrobenzenes - therapeutic use ; NS-398 ; Oxygenase ; p38 Mitogen-Activated Protein Kinases - metabolism ; Pancreatic cancer ; pancreatic cancer cell ; Pancreatic Neoplasms - drug therapy ; Pancreatic Neoplasms - enzymology ; Pancreatic Neoplasms - pathology ; Properties ; Prostaglandin endoperoxide synthase ; Proteins ; Pyridines - pharmacology ; RNA, Small Interfering - metabolism ; siRNA ; Studies ; Sulfonamides - pharmacology ; Sulfonamides - therapeutic use ; Western blotting</subject><ispartof>Molecular medicine reports, 2016-03, Vol.13 (3), p.2208-2214</ispartof><rights>Copyright © 2016, Spandidos Publications</rights><rights>COPYRIGHT 2016 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c525t-6ecf368d5de4cc34335ca8991e480d6dcc50acedd93dee552d571ad9e1d3409c3</citedby><cites>FETCH-LOGICAL-c525t-6ecf368d5de4cc34335ca8991e480d6dcc50acedd93dee552d571ad9e1d3409c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,5555,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26782265$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>LIU, HUA</creatorcontrib><creatorcontrib>XU, XUAN-FU</creatorcontrib><creatorcontrib>ZHAO, YAN</creatorcontrib><creatorcontrib>TANG, MAO-CHUN</creatorcontrib><creatorcontrib>ZHOU, YING-QUN</creatorcontrib><creatorcontrib>GAO, FENG-HOU</creatorcontrib><title>NS-398 promotes pancreatic cancer cell invasion by CD147 and MMP-2 via the activation of P38</title><title>Molecular medicine reports</title><addtitle>Mol Med Rep</addtitle><description>The overexpression or abnormal activation of cyclo-oxygenase-2 (COX-2) has been reported in pancreatic cancer cells. NS-398, a selective inhibitor of COX-2, is unable to inhibit pancreatic cancer cell proliferation, as determined by a Cell Counting Kit 8 assay. However, it does increase cancer cell invasiveness, and therefore the invasiveness of the PANC-1 cells was determined, along with the activation of P38, which was assessed by western blotting. In the present study, to evaluate the mechanisms underlying the action of NS-398 in pancreatic cancer cells, PANC-1 cells were treated with NS-398, and the invasion signaling pathways of cluster of differentiation (CD)147-matrix metalloproteinase (MMP)-2 and mitogen-activated protein kinases were evaluated. The results showed that NS-398-induced the expression of CD147 and MMP-2 via the activation of P38, which was involved in antiproliferative activity and induced pancreatic cancer cell invasiveness. The PANC-1 cells were also co-treated with CD147 small interfering (si)RNA and NS-398, and it was found that the NS-398-induced activation of P38 was not inhibited by CD147 siRNA, however, the expression of MMP-2 was inhibited. CD147 siRNA inhibited the invasiveness of the pancreatic cancer cells induced by NS-398, but also restored NS-398-induced antiproliferative activity. These data indicated that P38 in the pancreatic cancer cells was non-specifically activated by NS-398. This activation induced the expression of CD147-MMP-2, opposed the antiproliferative activity of NS-398 and increased the invasiveness of the PANC-1 cells.</description><subject>Basigin - metabolism</subject><subject>Cadmium</subject><subject>CD147 antigen</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - drug effects</subject><subject>cluster of differentiation 147</subject><subject>Cyclooxygenase-2</subject><subject>Cyclooxygenases</subject><subject>Development and progression</subject><subject>Enzyme Activation - drug effects</subject><subject>Enzymes</subject><subject>Gelatinase A</subject><subject>Gene expression</subject><subject>Genetic aspects</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Imidazoles - pharmacology</subject><subject>invasion</subject><subject>Invasiveness</subject><subject>Laboratories</subject><subject>MAP Kinase Signaling System - drug effects</subject><subject>Matrix metalloproteinase</subject><subject>Matrix Metalloproteinase 2 - metabolism</subject><subject>matrix metalloproteinase-2</subject><subject>Medical prognosis</subject><subject>Metalloproteinase</subject><subject>Metastasis</subject><subject>Neoplasm Invasiveness</subject><subject>Nitrobenzenes - pharmacology</subject><subject>Nitrobenzenes - therapeutic use</subject><subject>NS-398</subject><subject>Oxygenase</subject><subject>p38 Mitogen-Activated Protein Kinases - metabolism</subject><subject>Pancreatic cancer</subject><subject>pancreatic cancer cell</subject><subject>Pancreatic Neoplasms - drug therapy</subject><subject>Pancreatic Neoplasms - enzymology</subject><subject>Pancreatic Neoplasms - pathology</subject><subject>Properties</subject><subject>Prostaglandin endoperoxide synthase</subject><subject>Proteins</subject><subject>Pyridines - pharmacology</subject><subject>RNA, Small Interfering - metabolism</subject><subject>siRNA</subject><subject>Studies</subject><subject>Sulfonamides - pharmacology</subject><subject>Sulfonamides - therapeutic use</subject><subject>Western blotting</subject><issn>1791-2997</issn><issn>1791-3004</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNptkV1rFDEUhgdR7IdeeisBL-xN1iQnk0kuy_pVaGtBvRNCmpzRlJ3JNpld6L9vxl0rFslFDuF5D294muYVZwvQRrwbhrwQjKuF7DQ8aQ55ZzgFxuTT_SyM6Q6ao1JuGFOtaM3z5kCoTguh2sPmx-VXCkaTdU5DmrCQtRt9RjdFT3wdMROPqxWJ49aVmEZyfUeW77nsiBsDubi4ooJsoyPTLyTOT3Fbk5VKPbkC_aJ51rtVwZf7-7j5_vHDt-Vnev7l09ny9Jz62meiCn0PSoc2oPQeJEDrnTaGo9QsqOB9y5zHEAwExLYVoe24CwZ5AMmMh-PmZLe3_uJ2g2WyQyxzbTdi2hTLu85owxWoir55hN6kTR5rO8sNCNkpDfCX-ulWaOPYpyk7Py-1p1JqKQX7TS3-Q9UTcIg-jdjH-v5PgO4CPqdSMvZ2nePg8p3lzM42bbVpZ5t2tln51_uym-sBwwP9R18F3u6AUrWFGFJ5YOomyoEyoEIwDfeC5KNl</recordid><startdate>20160301</startdate><enddate>20160301</enddate><creator>LIU, HUA</creator><creator>XU, XUAN-FU</creator><creator>ZHAO, YAN</creator><creator>TANG, MAO-CHUN</creator><creator>ZHOU, YING-QUN</creator><creator>GAO, FENG-HOU</creator><general>D.A. Spandidos</general><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</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>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</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>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20160301</creationdate><title>NS-398 promotes pancreatic cancer cell invasion by CD147 and MMP-2 via the activation of P38</title><author>LIU, HUA ; XU, XUAN-FU ; ZHAO, YAN ; TANG, MAO-CHUN ; ZHOU, YING-QUN ; GAO, FENG-HOU</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c525t-6ecf368d5de4cc34335ca8991e480d6dcc50acedd93dee552d571ad9e1d3409c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Basigin - metabolism</topic><topic>Cadmium</topic><topic>CD147 antigen</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell proliferation</topic><topic>Cell Proliferation - drug effects</topic><topic>cluster of differentiation 147</topic><topic>Cyclooxygenase-2</topic><topic>Cyclooxygenases</topic><topic>Development and progression</topic><topic>Enzyme Activation - drug effects</topic><topic>Enzymes</topic><topic>Gelatinase A</topic><topic>Gene expression</topic><topic>Genetic aspects</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Imidazoles - pharmacology</topic><topic>invasion</topic><topic>Invasiveness</topic><topic>Laboratories</topic><topic>MAP Kinase Signaling System - drug effects</topic><topic>Matrix metalloproteinase</topic><topic>Matrix Metalloproteinase 2 - metabolism</topic><topic>matrix metalloproteinase-2</topic><topic>Medical prognosis</topic><topic>Metalloproteinase</topic><topic>Metastasis</topic><topic>Neoplasm Invasiveness</topic><topic>Nitrobenzenes - pharmacology</topic><topic>Nitrobenzenes - therapeutic use</topic><topic>NS-398</topic><topic>Oxygenase</topic><topic>p38 Mitogen-Activated Protein Kinases - metabolism</topic><topic>Pancreatic cancer</topic><topic>pancreatic cancer cell</topic><topic>Pancreatic Neoplasms - drug therapy</topic><topic>Pancreatic Neoplasms - enzymology</topic><topic>Pancreatic Neoplasms - pathology</topic><topic>Properties</topic><topic>Prostaglandin endoperoxide synthase</topic><topic>Proteins</topic><topic>Pyridines - pharmacology</topic><topic>RNA, Small Interfering - metabolism</topic><topic>siRNA</topic><topic>Studies</topic><topic>Sulfonamides - pharmacology</topic><topic>Sulfonamides - therapeutic use</topic><topic>Western blotting</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>LIU, HUA</creatorcontrib><creatorcontrib>XU, XUAN-FU</creatorcontrib><creatorcontrib>ZHAO, YAN</creatorcontrib><creatorcontrib>TANG, MAO-CHUN</creatorcontrib><creatorcontrib>ZHOU, YING-QUN</creatorcontrib><creatorcontrib>GAO, FENG-HOU</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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</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>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</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>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>Biological Science 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>MEDLINE - Academic</collection><jtitle>Molecular medicine reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>LIU, HUA</au><au>XU, XUAN-FU</au><au>ZHAO, YAN</au><au>TANG, MAO-CHUN</au><au>ZHOU, YING-QUN</au><au>GAO, FENG-HOU</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>NS-398 promotes pancreatic cancer cell invasion by CD147 and MMP-2 via the activation of P38</atitle><jtitle>Molecular medicine reports</jtitle><addtitle>Mol Med Rep</addtitle><date>2016-03-01</date><risdate>2016</risdate><volume>13</volume><issue>3</issue><spage>2208</spage><epage>2214</epage><pages>2208-2214</pages><issn>1791-2997</issn><eissn>1791-3004</eissn><abstract>The overexpression or abnormal activation of cyclo-oxygenase-2 (COX-2) has been reported in pancreatic cancer cells. NS-398, a selective inhibitor of COX-2, is unable to inhibit pancreatic cancer cell proliferation, as determined by a Cell Counting Kit 8 assay. However, it does increase cancer cell invasiveness, and therefore the invasiveness of the PANC-1 cells was determined, along with the activation of P38, which was assessed by western blotting. In the present study, to evaluate the mechanisms underlying the action of NS-398 in pancreatic cancer cells, PANC-1 cells were treated with NS-398, and the invasion signaling pathways of cluster of differentiation (CD)147-matrix metalloproteinase (MMP)-2 and mitogen-activated protein kinases were evaluated. The results showed that NS-398-induced the expression of CD147 and MMP-2 via the activation of P38, which was involved in antiproliferative activity and induced pancreatic cancer cell invasiveness. The PANC-1 cells were also co-treated with CD147 small interfering (si)RNA and NS-398, and it was found that the NS-398-induced activation of P38 was not inhibited by CD147 siRNA, however, the expression of MMP-2 was inhibited. CD147 siRNA inhibited the invasiveness of the pancreatic cancer cells induced by NS-398, but also restored NS-398-induced antiproliferative activity. These data indicated that P38 in the pancreatic cancer cells was non-specifically activated by NS-398. This activation induced the expression of CD147-MMP-2, opposed the antiproliferative activity of NS-398 and increased the invasiveness of the PANC-1 cells.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>26782265</pmid><doi>10.3892/mmr.2016.4783</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| source | Spandidos Publications Journals; MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Basigin - metabolism Cadmium CD147 antigen Cell growth Cell Line, Tumor Cell proliferation Cell Proliferation - drug effects cluster of differentiation 147 Cyclooxygenase-2 Cyclooxygenases Development and progression Enzyme Activation - drug effects Enzymes Gelatinase A Gene expression Genetic aspects Health aspects Humans Imidazoles - pharmacology invasion Invasiveness Laboratories MAP Kinase Signaling System - drug effects Matrix metalloproteinase Matrix Metalloproteinase 2 - metabolism matrix metalloproteinase-2 Medical prognosis Metalloproteinase Metastasis Neoplasm Invasiveness Nitrobenzenes - pharmacology Nitrobenzenes - therapeutic use NS-398 Oxygenase p38 Mitogen-Activated Protein Kinases - metabolism Pancreatic cancer pancreatic cancer cell Pancreatic Neoplasms - drug therapy Pancreatic Neoplasms - enzymology Pancreatic Neoplasms - pathology Properties Prostaglandin endoperoxide synthase Proteins Pyridines - pharmacology RNA, Small Interfering - metabolism siRNA Studies Sulfonamides - pharmacology Sulfonamides - therapeutic use Western blotting |
| title | NS-398 promotes pancreatic cancer cell invasion by CD147 and MMP-2 via the activation of P38 |
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