Thymoquinone reduces migration and invasion of human glioblastoma cells associated with FAK, MMP-2 and MMP-9 down-regulation
Summary Glioblastoma represent the most frequent primary tumors of the central nervous system and remain among the most aggressive human cancers as available therapeutic approaches still fail to contain their invasiveness. Many studies have reported elevated expression of the Focal Adhesion Kinase (...
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| Veröffentlicht in: | Investigational new drugs 2012-12, Vol.30 (6), p.2121-2131 |
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| creator | Kolli-Bouhafs, Kaouther Boukhari, Abdelaziz Abusnina, Abdurazzag Velot, Emilie Gies, Jean-Pierre Lugnier, Claire Rondé, Philippe |
| description | Summary
Glioblastoma represent the most frequent primary tumors of the central nervous system and remain among the most aggressive human cancers as available therapeutic approaches still fail to contain their invasiveness. Many studies have reported elevated expression of the Focal Adhesion Kinase (FAK) protein in glioblastoma, associated with an increase in the rates of both migration and invasion. This designates FAK as a promising target to limit invasiveness in glioblastoma. Thymoquinone (TQ), the main phytoactive compound of
Nigella sativa
has shown remarkable anti-neoplasic activities on a variety of cancer cells. Here, we studied the anti-invasive and anti-migratory effects of TQ on human glioblastoma cells. The results obtained indicated that TQ treatment reduced migration, adhesion and invasion of both U-87 and CCF-STTG1 cells. This was accompanied by a drastic down-regulation of FAK, associated with a reduction of ERK phosphorylation as well as MMP-2 and MMP-9 secretion. This study provides new data on FAK regulation by a natural product (TQ) which could be of a great value for the development of novel therapies in glioblastoma. |
| doi_str_mv | 10.1007/s10637-011-9777-3 |
| format | Article |
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Glioblastoma represent the most frequent primary tumors of the central nervous system and remain among the most aggressive human cancers as available therapeutic approaches still fail to contain their invasiveness. Many studies have reported elevated expression of the Focal Adhesion Kinase (FAK) protein in glioblastoma, associated with an increase in the rates of both migration and invasion. This designates FAK as a promising target to limit invasiveness in glioblastoma. Thymoquinone (TQ), the main phytoactive compound of
Nigella sativa
has shown remarkable anti-neoplasic activities on a variety of cancer cells. Here, we studied the anti-invasive and anti-migratory effects of TQ on human glioblastoma cells. The results obtained indicated that TQ treatment reduced migration, adhesion and invasion of both U-87 and CCF-STTG1 cells. This was accompanied by a drastic down-regulation of FAK, associated with a reduction of ERK phosphorylation as well as MMP-2 and MMP-9 secretion. This study provides new data on FAK regulation by a natural product (TQ) which could be of a great value for the development of novel therapies in glioblastoma.</description><identifier>ISSN: 0167-6997</identifier><identifier>EISSN: 1573-0646</identifier><identifier>DOI: 10.1007/s10637-011-9777-3</identifier><identifier>PMID: 22170088</identifier><identifier>CODEN: INNDDK</identifier><language>eng</language><publisher>Boston: Springer US</publisher><subject>Adhesion ; Antibodies ; Antineoplastic Agents, Phytogenic - pharmacology ; Benzoquinones - pharmacology ; Binding sites ; Biochemistry, Molecular Biology ; Brain cancer ; Cancer therapies ; Cell adhesion & migration ; Cell Adhesion - drug effects ; Cell growth ; Cell Line ; Cell Line, Tumor ; Cell Movement - drug effects ; Cellular Biology ; Down-Regulation ; Fibroblasts ; Fibroblasts - drug effects ; Fibroblasts - physiology ; Focal Adhesion Kinase 1 - metabolism ; Glioblastoma ; Glioma ; Humans ; Kinases ; Life Sciences ; Matrix Metalloproteinase 2 - metabolism ; Matrix Metalloproteinase 9 - metabolism ; Medical prognosis ; Medicine ; Medicine & Public Health ; Neoplasm Invasiveness ; Nervous system ; Nigella sativa ; Oncology ; Penicillin ; Pharmacology ; Pharmacology/Toxicology ; Phosphorylation ; Preclinical Studies ; Studies ; Tumors</subject><ispartof>Investigational new drugs, 2012-12, Vol.30 (6), p.2121-2131</ispartof><rights>Springer Science+Business Media, LLC 2011</rights><rights>Springer Science+Business Media New York 2012</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c406t-e246c84063313723da7c61d6ec9c311a912104478b53c8a084426d9f07b942e93</citedby><cites>FETCH-LOGICAL-c406t-e246c84063313723da7c61d6ec9c311a912104478b53c8a084426d9f07b942e93</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/s10637-011-9777-3$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10637-011-9777-3$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,314,776,780,881,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22170088$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-00783642$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Kolli-Bouhafs, Kaouther</creatorcontrib><creatorcontrib>Boukhari, Abdelaziz</creatorcontrib><creatorcontrib>Abusnina, Abdurazzag</creatorcontrib><creatorcontrib>Velot, Emilie</creatorcontrib><creatorcontrib>Gies, Jean-Pierre</creatorcontrib><creatorcontrib>Lugnier, Claire</creatorcontrib><creatorcontrib>Rondé, Philippe</creatorcontrib><title>Thymoquinone reduces migration and invasion of human glioblastoma cells associated with FAK, MMP-2 and MMP-9 down-regulation</title><title>Investigational new drugs</title><addtitle>Invest New Drugs</addtitle><addtitle>Invest New Drugs</addtitle><description>Summary
Glioblastoma represent the most frequent primary tumors of the central nervous system and remain among the most aggressive human cancers as available therapeutic approaches still fail to contain their invasiveness. Many studies have reported elevated expression of the Focal Adhesion Kinase (FAK) protein in glioblastoma, associated with an increase in the rates of both migration and invasion. This designates FAK as a promising target to limit invasiveness in glioblastoma. Thymoquinone (TQ), the main phytoactive compound of
Nigella sativa
has shown remarkable anti-neoplasic activities on a variety of cancer cells. Here, we studied the anti-invasive and anti-migratory effects of TQ on human glioblastoma cells. The results obtained indicated that TQ treatment reduced migration, adhesion and invasion of both U-87 and CCF-STTG1 cells. This was accompanied by a drastic down-regulation of FAK, associated with a reduction of ERK phosphorylation as well as MMP-2 and MMP-9 secretion. This study provides new data on FAK regulation by a natural product (TQ) which could be of a great value for the development of novel therapies in glioblastoma.</description><subject>Adhesion</subject><subject>Antibodies</subject><subject>Antineoplastic Agents, Phytogenic - pharmacology</subject><subject>Benzoquinones - pharmacology</subject><subject>Binding sites</subject><subject>Biochemistry, Molecular Biology</subject><subject>Brain cancer</subject><subject>Cancer therapies</subject><subject>Cell adhesion & migration</subject><subject>Cell Adhesion - drug effects</subject><subject>Cell growth</subject><subject>Cell Line</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement - drug effects</subject><subject>Cellular Biology</subject><subject>Down-Regulation</subject><subject>Fibroblasts</subject><subject>Fibroblasts - drug effects</subject><subject>Fibroblasts - physiology</subject><subject>Focal Adhesion Kinase 1 - metabolism</subject><subject>Glioblastoma</subject><subject>Glioma</subject><subject>Humans</subject><subject>Kinases</subject><subject>Life Sciences</subject><subject>Matrix Metalloproteinase 2 - metabolism</subject><subject>Matrix Metalloproteinase 9 - metabolism</subject><subject>Medical prognosis</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Neoplasm Invasiveness</subject><subject>Nervous system</subject><subject>Nigella sativa</subject><subject>Oncology</subject><subject>Penicillin</subject><subject>Pharmacology</subject><subject>Pharmacology/Toxicology</subject><subject>Phosphorylation</subject><subject>Preclinical Studies</subject><subject>Studies</subject><subject>Tumors</subject><issn>0167-6997</issn><issn>1573-0646</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kVFvFCEUhYnR2LX6A3wxJL7URJQLDAyPm8Za4zb6UJ8Jy7C7NDNQYaZNE3-8TKc2xsQnLvDdA_cchF4D_QCUqo8FqOSKUACilVKEP0EraBQnVAr5FK0oSEWk1uoIvSjlilLKtRLP0RFjoCht2xX6dXm4G9LPKcQUPc6-m5wveAj7bMeQIraxwyHe2DJv0g4fpsFGvO9D2va2jGmw2Pm-L9iWklywo-_wbRgP-Gz99T2-uPhO2L3GXGncpdtIst9P_b36S_RsZ_viXz2sx-jH2afL03Oy-fb5y-l6Q5ygciSeCenaWnIOXDHeWeUkdNI77TiA1cCACqHabcNda2krBJOd3lG11YJ5zY_Ru0X3YHtzncNg851JNpjz9cbMZ9XMlkvBbqCyJwt7nastvoxmCGUe0UafpmIAWMOapsIVffsPepWmHOskMwXVd1CiUrBQLqdSst89_gComWM0S4ymxmjmGA2vPW8elKft4LvHjj-5VYAtQKlXce_zX0__V_U3KGilIQ</recordid><startdate>20121201</startdate><enddate>20121201</enddate><creator>Kolli-Bouhafs, Kaouther</creator><creator>Boukhari, Abdelaziz</creator><creator>Abusnina, Abdurazzag</creator><creator>Velot, Emilie</creator><creator>Gies, Jean-Pierre</creator><creator>Lugnier, Claire</creator><creator>Rondé, Philippe</creator><general>Springer US</general><general>Springer Nature B.V</general><general>Springer Verlag</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>7QO</scope><scope>7RV</scope><scope>7WY</scope><scope>7WZ</scope><scope>7X7</scope><scope>7XB</scope><scope>87Z</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8FL</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>BEZIV</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FRNLG</scope><scope>FYUFA</scope><scope>F~G</scope><scope>GHDGH</scope><scope>K60</scope><scope>K6~</scope><scope>K9-</scope><scope>K9.</scope><scope>KB0</scope><scope>L.-</scope><scope>M0C</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>P64</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PJZUB</scope><scope>PKEHL</scope><scope>PPXIY</scope><scope>PQBIZ</scope><scope>PQBZA</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><scope>1XC</scope></search><sort><creationdate>20121201</creationdate><title>Thymoquinone reduces migration and invasion of human glioblastoma cells associated with FAK, MMP-2 and MMP-9 down-regulation</title><author>Kolli-Bouhafs, Kaouther ; Boukhari, Abdelaziz ; Abusnina, Abdurazzag ; Velot, Emilie ; Gies, Jean-Pierre ; Lugnier, Claire ; Rondé, Philippe</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c406t-e246c84063313723da7c61d6ec9c311a912104478b53c8a084426d9f07b942e93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Adhesion</topic><topic>Antibodies</topic><topic>Antineoplastic Agents, Phytogenic - pharmacology</topic><topic>Benzoquinones - pharmacology</topic><topic>Binding sites</topic><topic>Biochemistry, Molecular Biology</topic><topic>Brain cancer</topic><topic>Cancer therapies</topic><topic>Cell adhesion & migration</topic><topic>Cell Adhesion - drug effects</topic><topic>Cell growth</topic><topic>Cell Line</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement - drug effects</topic><topic>Cellular Biology</topic><topic>Down-Regulation</topic><topic>Fibroblasts</topic><topic>Fibroblasts - drug effects</topic><topic>Fibroblasts - physiology</topic><topic>Focal Adhesion Kinase 1 - metabolism</topic><topic>Glioblastoma</topic><topic>Glioma</topic><topic>Humans</topic><topic>Kinases</topic><topic>Life Sciences</topic><topic>Matrix Metalloproteinase 2 - metabolism</topic><topic>Matrix Metalloproteinase 9 - metabolism</topic><topic>Medical prognosis</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Neoplasm Invasiveness</topic><topic>Nervous system</topic><topic>Nigella sativa</topic><topic>Oncology</topic><topic>Penicillin</topic><topic>Pharmacology</topic><topic>Pharmacology/Toxicology</topic><topic>Phosphorylation</topic><topic>Preclinical Studies</topic><topic>Studies</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kolli-Bouhafs, Kaouther</creatorcontrib><creatorcontrib>Boukhari, Abdelaziz</creatorcontrib><creatorcontrib>Abusnina, Abdurazzag</creatorcontrib><creatorcontrib>Velot, Emilie</creatorcontrib><creatorcontrib>Gies, Jean-Pierre</creatorcontrib><creatorcontrib>Lugnier, Claire</creatorcontrib><creatorcontrib>Rondé, Philippe</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>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>ABI/INFORM Collection</collection><collection>ABI/INFORM Global (PDF only)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>ABI/INFORM Global (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ABI/INFORM Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>Business Premium Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Business Premium Collection (Alumni)</collection><collection>Health Research Premium Collection</collection><collection>ABI/INFORM Global (Corporate)</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Business Collection (Alumni Edition)</collection><collection>ProQuest Business Collection</collection><collection>Consumer Health Database (Alumni Edition)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ABI/INFORM Professional Advanced</collection><collection>ABI/INFORM Global</collection><collection>Consumer Health Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest Central (New)</collection><collection>ProQuest One Academic (New)</collection><collection>ProQuest Health & Medical Research Collection</collection><collection>ProQuest One Academic Middle East (New)</collection><collection>ProQuest One Health & Nursing</collection><collection>ProQuest One Business</collection><collection>ProQuest One Business (Alumni)</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 Basic</collection><collection>MEDLINE - Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><jtitle>Investigational new drugs</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kolli-Bouhafs, Kaouther</au><au>Boukhari, Abdelaziz</au><au>Abusnina, Abdurazzag</au><au>Velot, Emilie</au><au>Gies, Jean-Pierre</au><au>Lugnier, Claire</au><au>Rondé, Philippe</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Thymoquinone reduces migration and invasion of human glioblastoma cells associated with FAK, MMP-2 and MMP-9 down-regulation</atitle><jtitle>Investigational new drugs</jtitle><stitle>Invest New Drugs</stitle><addtitle>Invest New Drugs</addtitle><date>2012-12-01</date><risdate>2012</risdate><volume>30</volume><issue>6</issue><spage>2121</spage><epage>2131</epage><pages>2121-2131</pages><issn>0167-6997</issn><eissn>1573-0646</eissn><coden>INNDDK</coden><abstract>Summary
Glioblastoma represent the most frequent primary tumors of the central nervous system and remain among the most aggressive human cancers as available therapeutic approaches still fail to contain their invasiveness. Many studies have reported elevated expression of the Focal Adhesion Kinase (FAK) protein in glioblastoma, associated with an increase in the rates of both migration and invasion. This designates FAK as a promising target to limit invasiveness in glioblastoma. Thymoquinone (TQ), the main phytoactive compound of
Nigella sativa
has shown remarkable anti-neoplasic activities on a variety of cancer cells. Here, we studied the anti-invasive and anti-migratory effects of TQ on human glioblastoma cells. The results obtained indicated that TQ treatment reduced migration, adhesion and invasion of both U-87 and CCF-STTG1 cells. This was accompanied by a drastic down-regulation of FAK, associated with a reduction of ERK phosphorylation as well as MMP-2 and MMP-9 secretion. This study provides new data on FAK regulation by a natural product (TQ) which could be of a great value for the development of novel therapies in glioblastoma.</abstract><cop>Boston</cop><pub>Springer US</pub><pmid>22170088</pmid><doi>10.1007/s10637-011-9777-3</doi><tpages>11</tpages></addata></record> |
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| ispartof | Investigational new drugs, 2012-12, Vol.30 (6), p.2121-2131 |
| issn | 0167-6997 1573-0646 |
| language | eng |
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| source | MEDLINE; Springer Nature - Complete Springer Journals |
| subjects | Adhesion Antibodies Antineoplastic Agents, Phytogenic - pharmacology Benzoquinones - pharmacology Binding sites Biochemistry, Molecular Biology Brain cancer Cancer therapies Cell adhesion & migration Cell Adhesion - drug effects Cell growth Cell Line Cell Line, Tumor Cell Movement - drug effects Cellular Biology Down-Regulation Fibroblasts Fibroblasts - drug effects Fibroblasts - physiology Focal Adhesion Kinase 1 - metabolism Glioblastoma Glioma Humans Kinases Life Sciences Matrix Metalloproteinase 2 - metabolism Matrix Metalloproteinase 9 - metabolism Medical prognosis Medicine Medicine & Public Health Neoplasm Invasiveness Nervous system Nigella sativa Oncology Penicillin Pharmacology Pharmacology/Toxicology Phosphorylation Preclinical Studies Studies Tumors |
| title | Thymoquinone reduces migration and invasion of human glioblastoma cells associated with FAK, MMP-2 and MMP-9 down-regulation |
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