Diallyl trisulfide inhibits migration, invasion and angiogenesis of human colon cancer HT‐29 cells and umbilical vein endothelial cells, and suppresses murine xenograft tumour growth
Angiogenesis inhibitors are beneficial for the prevention and treatment of angiogenesis‐dependent diseases including cancer. We examined the cytotoxic, anti‐metastatic, anti‐cancer and anti‐angiogenic effects of diallyl trisulfide (DATS). In HT29 cells, DATS inhibited migration and invasion through...
Gespeichert in:
| Veröffentlicht in: | Journal of cellular and molecular medicine 2015-02, Vol.19 (2), p.474-484 |
|---|---|
| Hauptverfasser: | , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 484 |
|---|---|
| container_issue | 2 |
| container_start_page | 474 |
| container_title | Journal of cellular and molecular medicine |
| container_volume | 19 |
| creator | Lai, Kuang‐Chi Hsu, Shu‐Chun Yang, Jai‐Sing Yu, Chien‐Chih Lein, Jin‐Cherng Chung, Jing‐Gung |
| description | Angiogenesis inhibitors are beneficial for the prevention and treatment of angiogenesis‐dependent diseases including cancer. We examined the cytotoxic, anti‐metastatic, anti‐cancer and anti‐angiogenic effects of diallyl trisulfide (DATS). In HT29 cells, DATS inhibited migration and invasion through the inhibition of focal adhesion kinase (FAK), extracellular signal‐regulated kinase, c‐Jun N‐terminal kinase and p38 which was associated with inhibition of matrix metalloproteinases‐2, ‐7 and ‐9 and VEGF. In human umbilical vein endothelial cells (HUVEC), DATS inhibited the migration and angiogenesis through FAK, Src and Ras. DATS also inhibited the secretion of VEGF. The capillary‐like tube structure formation and migration by HUVEC was inhibited by DATS. The chicken egg chorioallantoic membrane (CAM) assay indicated that DATS treatment inhibited ex‐vivo angiogenesis. We investigated the anti‐tumour effects of DATS against human colon cancer xenografts in BALB/cnu/nu mice and its anti‐angiogenic activity in vivo. In this in‐vivo study, DATS also inhibited the tumour growth, tumour weight and angiogenesis (decreased the levels of haemoglobin) in HT29 cells. In conclusion, the present results suggest that the inhibition of angiogenesis may be an important mechanism in colon cancer chemotherapy by DATS. |
| doi_str_mv | 10.1111/jcmm.12486 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4407594</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2290369347</sourcerecordid><originalsourceid>FETCH-LOGICAL-c5186-7440d3c0e3142bcb3ecd0a1ef4afbf4faf524dfe39fc73629517cf7553f47d533</originalsourceid><addsrcrecordid>eNp9kkuO1DAQhiMEYh6w4QDIEhs0mh7i2HltRkLNY0AzYjOsLccpJ245dmMnPfSOI3AczsNJqO40I2CBJcsl-_Nff6kqSZ7R9ILierVSw3BBM14VD5JjmlfZgteMPzzEtGLVUXIS4ypNWUFZ_Tg5ynKOMWfHyY83Rlq7tWQMJk5WmxaIcb1pzBjJYLogR-PdOd5tZMSISNfi7ozvwEE0kXhN-mmQjihv8V1JpyCQq9uf375nNVFgbdx_mobGWKOkJRswjoBr_diDxfQzdL6n4rReB4gRMPsUjAPyFZxHG3ok4zT4KZAu-Luxf5I80tJGeHo4T5PP797eLq8W15_ef1i-vl6onFbFouQ8bZlKgVGeNaphoNpUUtBc6kZzLXWe8VYDq7UqWZHVOS2VLvOcaV62OWOnyeWsu56aAVoFbgzSinUwgwxb4aURf78404vObwQmLvOao8DLg0DwXyaIoxhM3FUsHfgpClqgA1bXVYXoi3_QFRbssDyRZTV2DNtaInU2Uyr4GAPoezM0FbuBELuBEPuBQPj5n_bv0d8TgACdgTtjYfsfKfFxeXMzi_4Cyq_HiQ</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2290369347</pqid></control><display><type>article</type><title>Diallyl trisulfide inhibits migration, invasion and angiogenesis of human colon cancer HT‐29 cells and umbilical vein endothelial cells, and suppresses murine xenograft tumour growth</title><source>MEDLINE</source><source>DOAJ Directory of Open Access Journals</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Access via Wiley Online Library</source><source>Wiley-Blackwell Open Access Titles</source><source>PubMed Central</source><creator>Lai, Kuang‐Chi ; Hsu, Shu‐Chun ; Yang, Jai‐Sing ; Yu, Chien‐Chih ; Lein, Jin‐Cherng ; Chung, Jing‐Gung</creator><creatorcontrib>Lai, Kuang‐Chi ; Hsu, Shu‐Chun ; Yang, Jai‐Sing ; Yu, Chien‐Chih ; Lein, Jin‐Cherng ; Chung, Jing‐Gung</creatorcontrib><description>Angiogenesis inhibitors are beneficial for the prevention and treatment of angiogenesis‐dependent diseases including cancer. We examined the cytotoxic, anti‐metastatic, anti‐cancer and anti‐angiogenic effects of diallyl trisulfide (DATS). In HT29 cells, DATS inhibited migration and invasion through the inhibition of focal adhesion kinase (FAK), extracellular signal‐regulated kinase, c‐Jun N‐terminal kinase and p38 which was associated with inhibition of matrix metalloproteinases‐2, ‐7 and ‐9 and VEGF. In human umbilical vein endothelial cells (HUVEC), DATS inhibited the migration and angiogenesis through FAK, Src and Ras. DATS also inhibited the secretion of VEGF. The capillary‐like tube structure formation and migration by HUVEC was inhibited by DATS. The chicken egg chorioallantoic membrane (CAM) assay indicated that DATS treatment inhibited ex‐vivo angiogenesis. We investigated the anti‐tumour effects of DATS against human colon cancer xenografts in BALB/cnu/nu mice and its anti‐angiogenic activity in vivo. In this in‐vivo study, DATS also inhibited the tumour growth, tumour weight and angiogenesis (decreased the levels of haemoglobin) in HT29 cells. In conclusion, the present results suggest that the inhibition of angiogenesis may be an important mechanism in colon cancer chemotherapy by DATS.</description><identifier>ISSN: 1582-1838</identifier><identifier>EISSN: 1582-4934</identifier><identifier>DOI: 10.1111/jcmm.12486</identifier><identifier>PMID: 25403643</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>Allyl Compounds - pharmacology ; Angiogenesis ; Angiogenesis inhibitors ; Angiogenesis Inhibitors - pharmacology ; Animals ; Cancer therapies ; Capillary tubes ; Cell adhesion & migration ; Cell growth ; Cell Line ; Cell Line, Tumor ; Cell migration ; Cell Movement - drug effects ; Cell Proliferation - drug effects ; Chemotherapy ; Chorioallantoic membrane ; Colon cancer ; Colorectal cancer ; Crop diseases ; Cytokines ; Cytotoxicity ; DATS ; Diallyl trisulfide ; Endothelial cells ; Focal adhesion kinase ; Gene expression ; Growth factors ; Hemoglobin ; HT29 Cells ; HT‐29 human colon adenocarcinoma cells ; Human Umbilical Vein Endothelial Cells - drug effects ; Humans ; HUVEC ; Industrial research ; Inhibition ; JNK protein ; Kinases ; Matrix metalloproteinase ; Medical treatment ; Metastases ; Metastasis ; Mice ; migration and invasion ; Neoplasm Invasiveness - prevention & control ; Neovascularization, Pathologic - drug therapy ; Original ; Poultry ; Proteins ; R&D ; Research & development ; Secretion ; Sulfides - pharmacology ; Tumors ; Umbilical vein ; Vascular endothelial growth factor ; Veins ; Veins & arteries ; Xenograft Model Antitumor Assays - methods ; Xenografts</subject><ispartof>Journal of cellular and molecular medicine, 2015-02, Vol.19 (2), p.474-484</ispartof><rights>2014 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.</rights><rights>2015. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2014 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine. 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5186-7440d3c0e3142bcb3ecd0a1ef4afbf4faf524dfe39fc73629517cf7553f47d533</citedby><cites>FETCH-LOGICAL-c5186-7440d3c0e3142bcb3ecd0a1ef4afbf4faf524dfe39fc73629517cf7553f47d533</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4407594/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4407594/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,865,886,1418,11564,27926,27927,45576,45577,46054,46478,53793,53795</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25403643$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lai, Kuang‐Chi</creatorcontrib><creatorcontrib>Hsu, Shu‐Chun</creatorcontrib><creatorcontrib>Yang, Jai‐Sing</creatorcontrib><creatorcontrib>Yu, Chien‐Chih</creatorcontrib><creatorcontrib>Lein, Jin‐Cherng</creatorcontrib><creatorcontrib>Chung, Jing‐Gung</creatorcontrib><title>Diallyl trisulfide inhibits migration, invasion and angiogenesis of human colon cancer HT‐29 cells and umbilical vein endothelial cells, and suppresses murine xenograft tumour growth</title><title>Journal of cellular and molecular medicine</title><addtitle>J Cell Mol Med</addtitle><description>Angiogenesis inhibitors are beneficial for the prevention and treatment of angiogenesis‐dependent diseases including cancer. We examined the cytotoxic, anti‐metastatic, anti‐cancer and anti‐angiogenic effects of diallyl trisulfide (DATS). In HT29 cells, DATS inhibited migration and invasion through the inhibition of focal adhesion kinase (FAK), extracellular signal‐regulated kinase, c‐Jun N‐terminal kinase and p38 which was associated with inhibition of matrix metalloproteinases‐2, ‐7 and ‐9 and VEGF. In human umbilical vein endothelial cells (HUVEC), DATS inhibited the migration and angiogenesis through FAK, Src and Ras. DATS also inhibited the secretion of VEGF. The capillary‐like tube structure formation and migration by HUVEC was inhibited by DATS. The chicken egg chorioallantoic membrane (CAM) assay indicated that DATS treatment inhibited ex‐vivo angiogenesis. We investigated the anti‐tumour effects of DATS against human colon cancer xenografts in BALB/cnu/nu mice and its anti‐angiogenic activity in vivo. In this in‐vivo study, DATS also inhibited the tumour growth, tumour weight and angiogenesis (decreased the levels of haemoglobin) in HT29 cells. In conclusion, the present results suggest that the inhibition of angiogenesis may be an important mechanism in colon cancer chemotherapy by DATS.</description><subject>Allyl Compounds - pharmacology</subject><subject>Angiogenesis</subject><subject>Angiogenesis inhibitors</subject><subject>Angiogenesis Inhibitors - pharmacology</subject><subject>Animals</subject><subject>Cancer therapies</subject><subject>Capillary tubes</subject><subject>Cell adhesion & migration</subject><subject>Cell growth</subject><subject>Cell Line</subject><subject>Cell Line, Tumor</subject><subject>Cell migration</subject><subject>Cell Movement - drug effects</subject><subject>Cell Proliferation - drug effects</subject><subject>Chemotherapy</subject><subject>Chorioallantoic membrane</subject><subject>Colon cancer</subject><subject>Colorectal cancer</subject><subject>Crop diseases</subject><subject>Cytokines</subject><subject>Cytotoxicity</subject><subject>DATS</subject><subject>Diallyl trisulfide</subject><subject>Endothelial cells</subject><subject>Focal adhesion kinase</subject><subject>Gene expression</subject><subject>Growth factors</subject><subject>Hemoglobin</subject><subject>HT29 Cells</subject><subject>HT‐29 human colon adenocarcinoma cells</subject><subject>Human Umbilical Vein Endothelial Cells - drug effects</subject><subject>Humans</subject><subject>HUVEC</subject><subject>Industrial research</subject><subject>Inhibition</subject><subject>JNK protein</subject><subject>Kinases</subject><subject>Matrix metalloproteinase</subject><subject>Medical treatment</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>Mice</subject><subject>migration and invasion</subject><subject>Neoplasm Invasiveness - prevention & control</subject><subject>Neovascularization, Pathologic - drug therapy</subject><subject>Original</subject><subject>Poultry</subject><subject>Proteins</subject><subject>R&D</subject><subject>Research & development</subject><subject>Secretion</subject><subject>Sulfides - pharmacology</subject><subject>Tumors</subject><subject>Umbilical vein</subject><subject>Vascular endothelial growth factor</subject><subject>Veins</subject><subject>Veins & arteries</subject><subject>Xenograft Model Antitumor Assays - methods</subject><subject>Xenografts</subject><issn>1582-1838</issn><issn>1582-4934</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><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>eNp9kkuO1DAQhiMEYh6w4QDIEhs0mh7i2HltRkLNY0AzYjOsLccpJ245dmMnPfSOI3AczsNJqO40I2CBJcsl-_Nff6kqSZ7R9ILierVSw3BBM14VD5JjmlfZgteMPzzEtGLVUXIS4ypNWUFZ_Tg5ynKOMWfHyY83Rlq7tWQMJk5WmxaIcb1pzBjJYLogR-PdOd5tZMSISNfi7ozvwEE0kXhN-mmQjihv8V1JpyCQq9uf375nNVFgbdx_mobGWKOkJRswjoBr_diDxfQzdL6n4rReB4gRMPsUjAPyFZxHG3ok4zT4KZAu-Luxf5I80tJGeHo4T5PP797eLq8W15_ef1i-vl6onFbFouQ8bZlKgVGeNaphoNpUUtBc6kZzLXWe8VYDq7UqWZHVOS2VLvOcaV62OWOnyeWsu56aAVoFbgzSinUwgwxb4aURf78404vObwQmLvOao8DLg0DwXyaIoxhM3FUsHfgpClqgA1bXVYXoi3_QFRbssDyRZTV2DNtaInU2Uyr4GAPoezM0FbuBELuBEPuBQPj5n_bv0d8TgACdgTtjYfsfKfFxeXMzi_4Cyq_HiQ</recordid><startdate>201502</startdate><enddate>201502</enddate><creator>Lai, Kuang‐Chi</creator><creator>Hsu, Shu‐Chun</creator><creator>Yang, Jai‐Sing</creator><creator>Yu, Chien‐Chih</creator><creator>Lein, Jin‐Cherng</creator><creator>Chung, Jing‐Gung</creator><general>John Wiley & Sons, Inc</general><general>BlackWell Publishing Ltd</general><scope>24P</scope><scope>WIN</scope><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>7QP</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</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>FR3</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>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>201502</creationdate><title>Diallyl trisulfide inhibits migration, invasion and angiogenesis of human colon cancer HT‐29 cells and umbilical vein endothelial cells, and suppresses murine xenograft tumour growth</title><author>Lai, Kuang‐Chi ; Hsu, Shu‐Chun ; Yang, Jai‐Sing ; Yu, Chien‐Chih ; Lein, Jin‐Cherng ; Chung, Jing‐Gung</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5186-7440d3c0e3142bcb3ecd0a1ef4afbf4faf524dfe39fc73629517cf7553f47d533</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Allyl Compounds - pharmacology</topic><topic>Angiogenesis</topic><topic>Angiogenesis inhibitors</topic><topic>Angiogenesis Inhibitors - pharmacology</topic><topic>Animals</topic><topic>Cancer therapies</topic><topic>Capillary tubes</topic><topic>Cell adhesion & migration</topic><topic>Cell growth</topic><topic>Cell Line</topic><topic>Cell Line, Tumor</topic><topic>Cell migration</topic><topic>Cell Movement - drug effects</topic><topic>Cell Proliferation - drug effects</topic><topic>Chemotherapy</topic><topic>Chorioallantoic membrane</topic><topic>Colon cancer</topic><topic>Colorectal cancer</topic><topic>Crop diseases</topic><topic>Cytokines</topic><topic>Cytotoxicity</topic><topic>DATS</topic><topic>Diallyl trisulfide</topic><topic>Endothelial cells</topic><topic>Focal adhesion kinase</topic><topic>Gene expression</topic><topic>Growth factors</topic><topic>Hemoglobin</topic><topic>HT29 Cells</topic><topic>HT‐29 human colon adenocarcinoma cells</topic><topic>Human Umbilical Vein Endothelial Cells - drug effects</topic><topic>Humans</topic><topic>HUVEC</topic><topic>Industrial research</topic><topic>Inhibition</topic><topic>JNK protein</topic><topic>Kinases</topic><topic>Matrix metalloproteinase</topic><topic>Medical treatment</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>Mice</topic><topic>migration and invasion</topic><topic>Neoplasm Invasiveness - prevention & control</topic><topic>Neovascularization, Pathologic - drug therapy</topic><topic>Original</topic><topic>Poultry</topic><topic>Proteins</topic><topic>R&D</topic><topic>Research & development</topic><topic>Secretion</topic><topic>Sulfides - pharmacology</topic><topic>Tumors</topic><topic>Umbilical vein</topic><topic>Vascular endothelial growth factor</topic><topic>Veins</topic><topic>Veins & arteries</topic><topic>Xenograft Model Antitumor Assays - methods</topic><topic>Xenografts</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lai, Kuang‐Chi</creatorcontrib><creatorcontrib>Hsu, Shu‐Chun</creatorcontrib><creatorcontrib>Yang, Jai‐Sing</creatorcontrib><creatorcontrib>Yu, Chien‐Chih</creatorcontrib><creatorcontrib>Lein, Jin‐Cherng</creatorcontrib><creatorcontrib>Chung, Jing‐Gung</creatorcontrib><collection>Wiley-Blackwell Open Access Titles</collection><collection>Wiley Online Library (Open Access Collection)</collection><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>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research 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>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>Engineering Research Database</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>Science Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</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 Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of cellular and molecular medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lai, Kuang‐Chi</au><au>Hsu, Shu‐Chun</au><au>Yang, Jai‐Sing</au><au>Yu, Chien‐Chih</au><au>Lein, Jin‐Cherng</au><au>Chung, Jing‐Gung</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Diallyl trisulfide inhibits migration, invasion and angiogenesis of human colon cancer HT‐29 cells and umbilical vein endothelial cells, and suppresses murine xenograft tumour growth</atitle><jtitle>Journal of cellular and molecular medicine</jtitle><addtitle>J Cell Mol Med</addtitle><date>2015-02</date><risdate>2015</risdate><volume>19</volume><issue>2</issue><spage>474</spage><epage>484</epage><pages>474-484</pages><issn>1582-1838</issn><eissn>1582-4934</eissn><abstract>Angiogenesis inhibitors are beneficial for the prevention and treatment of angiogenesis‐dependent diseases including cancer. We examined the cytotoxic, anti‐metastatic, anti‐cancer and anti‐angiogenic effects of diallyl trisulfide (DATS). In HT29 cells, DATS inhibited migration and invasion through the inhibition of focal adhesion kinase (FAK), extracellular signal‐regulated kinase, c‐Jun N‐terminal kinase and p38 which was associated with inhibition of matrix metalloproteinases‐2, ‐7 and ‐9 and VEGF. In human umbilical vein endothelial cells (HUVEC), DATS inhibited the migration and angiogenesis through FAK, Src and Ras. DATS also inhibited the secretion of VEGF. The capillary‐like tube structure formation and migration by HUVEC was inhibited by DATS. The chicken egg chorioallantoic membrane (CAM) assay indicated that DATS treatment inhibited ex‐vivo angiogenesis. We investigated the anti‐tumour effects of DATS against human colon cancer xenografts in BALB/cnu/nu mice and its anti‐angiogenic activity in vivo. In this in‐vivo study, DATS also inhibited the tumour growth, tumour weight and angiogenesis (decreased the levels of haemoglobin) in HT29 cells. In conclusion, the present results suggest that the inhibition of angiogenesis may be an important mechanism in colon cancer chemotherapy by DATS.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>25403643</pmid><doi>10.1111/jcmm.12486</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1582-1838 |
| ispartof | Journal of cellular and molecular medicine, 2015-02, Vol.19 (2), p.474-484 |
| issn | 1582-1838 1582-4934 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4407594 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Access via Wiley Online Library; Wiley-Blackwell Open Access Titles; PubMed Central |
| subjects | Allyl Compounds - pharmacology Angiogenesis Angiogenesis inhibitors Angiogenesis Inhibitors - pharmacology Animals Cancer therapies Capillary tubes Cell adhesion & migration Cell growth Cell Line Cell Line, Tumor Cell migration Cell Movement - drug effects Cell Proliferation - drug effects Chemotherapy Chorioallantoic membrane Colon cancer Colorectal cancer Crop diseases Cytokines Cytotoxicity DATS Diallyl trisulfide Endothelial cells Focal adhesion kinase Gene expression Growth factors Hemoglobin HT29 Cells HT‐29 human colon adenocarcinoma cells Human Umbilical Vein Endothelial Cells - drug effects Humans HUVEC Industrial research Inhibition JNK protein Kinases Matrix metalloproteinase Medical treatment Metastases Metastasis Mice migration and invasion Neoplasm Invasiveness - prevention & control Neovascularization, Pathologic - drug therapy Original Poultry Proteins R&D Research & development Secretion Sulfides - pharmacology Tumors Umbilical vein Vascular endothelial growth factor Veins Veins & arteries Xenograft Model Antitumor Assays - methods Xenografts |
| title | Diallyl trisulfide inhibits migration, invasion and angiogenesis of human colon cancer HT‐29 cells and umbilical vein endothelial cells, and suppresses murine xenograft tumour growth |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-18T05%3A35%3A15IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Diallyl%20trisulfide%20inhibits%20migration,%20invasion%20and%20angiogenesis%20of%20human%20colon%20cancer%20HT%E2%80%9029%20cells%20and%20umbilical%20vein%20endothelial%20cells,%20and%20suppresses%20murine%20xenograft%20tumour%20growth&rft.jtitle=Journal%20of%20cellular%20and%20molecular%20medicine&rft.au=Lai,%20Kuang%E2%80%90Chi&rft.date=2015-02&rft.volume=19&rft.issue=2&rft.spage=474&rft.epage=484&rft.pages=474-484&rft.issn=1582-1838&rft.eissn=1582-4934&rft_id=info:doi/10.1111/jcmm.12486&rft_dat=%3Cproquest_pubme%3E2290369347%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2290369347&rft_id=info:pmid/25403643&rfr_iscdi=true |