Brucine suppresses colon cancer cells growth via mediating KDR signalling pathway
Angiogenesis plays an important role in colon cancer development. This study aimed to demonstrate the effect of brucine on tumour angiogenesis and its mechanism of action. The anti‐angiogenic effect was evaluated on the chicken chorioallantoic membrane (CAM) model and tube formation. The mechanism w...
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| Veröffentlicht in: | Journal of cellular and molecular medicine 2013-10, Vol.17 (10), p.1316-1324 |
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| description | Angiogenesis plays an important role in colon cancer development. This study aimed to demonstrate the effect of brucine on tumour angiogenesis and its mechanism of action. The anti‐angiogenic effect was evaluated on the chicken chorioallantoic membrane (CAM) model and tube formation. The mechanism was demonstrated through detecting mRNA and protein expressions of VEGFR2 (KDR), PKCα, PLCγ and Raf1 by reverse transcription‐polymerase chain reaction (RT‐PCR) and Western blot (WB), as well as expressions of VEGF and PKCβ and mTOR by ELISA and WB. The results showed that brucine significantly reduced angiogenesis of CAM and tube formation, inhibited the VEGF secretion and mTOR expression in LoVo cell and down‐regulated the mRNA and phosphorylation protein expressions of KDR, PKCα, PLCγ and Raf1. In addition, the effects of brucine on KDR kinase activity, viability of LoVo cell and gene knockdown cell were detected with the Lance™ assay, WST‐1 assay and instantaneous siRNA. Compared to that of normal LoVo cells, the inhibition on proliferation of knockdown cells by brucine decreased significantly. These results suggest that brucine could inhibit angiogenesis and be a useful therapeutic candidate for colon cancer intervention. |
| doi_str_mv | 10.1111/jcmm.12108 |
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| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4159018</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2299168626</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4488-c9a29622dc6681edefb4edef34b200a5c91d75726be1fc774b53aef058b04b053</originalsourceid><addsrcrecordid>eNp9kE9PwyAYh4nROJ1e_ACGxJtJJ1BK4WKi879bjEbPhDK6sXRthXbLvr2tnYte5PDCG578eHkAOMFogJt1MdeLxQATjPgOOMARJwEVId3dnDEPeQ8cej9HKGQ4FPugR0KBIhazA_B67WptcwN9XZbOeG881EVW5FCrXBsHtckyD6euWFUzuLQKLszEqsrmU_h88wa9neYqy9q2VNVspdZHYC9VmTfHm70PPu5u34cPwejl_nF4NQo0pZwHWigiGCETzRjHZmLShLY1pAlBSEVa4EkcxYQlBqc6jmkShcqkKOIJogmKwj647HLLOmlm0iavnMpk6exCubUslJV_b3I7k9NiKSmOBGqs9MHZJsAVn7XxlZwXtWt-4yUhQmDGGWENdd5R2hXeO5NuX8BItvplq19-62_g098zbdEf3w2AO2BlM7P-J0o-DcfjLvQLsLKRzg</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2299168626</pqid></control><display><type>article</type><title>Brucine suppresses colon cancer cells growth via mediating KDR signalling pathway</title><source>MEDLINE</source><source>DOAJ Directory of Open Access Journals</source><source>Wiley Online Library Journals Frontfile Complete</source><source>Wiley Online Library Open Access</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><creator>Luo, Wenjuan ; Wang, Xiaoli ; Zheng, Lei ; Zhan, Yingzhuan ; Zhang, Dongdong ; Zhang, Jie ; Zhang, Yanmin</creator><creatorcontrib>Luo, Wenjuan ; Wang, Xiaoli ; Zheng, Lei ; Zhan, Yingzhuan ; Zhang, Dongdong ; Zhang, Jie ; Zhang, Yanmin</creatorcontrib><description>Angiogenesis plays an important role in colon cancer development. This study aimed to demonstrate the effect of brucine on tumour angiogenesis and its mechanism of action. The anti‐angiogenic effect was evaluated on the chicken chorioallantoic membrane (CAM) model and tube formation. The mechanism was demonstrated through detecting mRNA and protein expressions of VEGFR2 (KDR), PKCα, PLCγ and Raf1 by reverse transcription‐polymerase chain reaction (RT‐PCR) and Western blot (WB), as well as expressions of VEGF and PKCβ and mTOR by ELISA and WB. The results showed that brucine significantly reduced angiogenesis of CAM and tube formation, inhibited the VEGF secretion and mTOR expression in LoVo cell and down‐regulated the mRNA and phosphorylation protein expressions of KDR, PKCα, PLCγ and Raf1. In addition, the effects of brucine on KDR kinase activity, viability of LoVo cell and gene knockdown cell were detected with the Lance™ assay, WST‐1 assay and instantaneous siRNA. Compared to that of normal LoVo cells, the inhibition on proliferation of knockdown cells by brucine decreased significantly. These results suggest that brucine could inhibit angiogenesis and be a useful therapeutic candidate for colon cancer intervention.</description><identifier>ISSN: 1582-1838</identifier><identifier>EISSN: 1582-4934</identifier><identifier>DOI: 10.1111/jcmm.12108</identifier><identifier>PMID: 23905676</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>Angiogenesis ; Apoptosis ; Base Sequence ; Brucine ; Cell adhesion & migration ; Cell Division - drug effects ; Cell growth ; Cell Line, Tumor ; Cell proliferation ; Chorioallantoic membrane ; Colon cancer ; Colonic Neoplasms - metabolism ; Colonic Neoplasms - pathology ; Colorectal cancer ; DNA Primers ; Enzyme-linked immunosorbent assay ; Humans ; KDR ; Kinases ; LoVo cells ; Original ; Phosphorylation ; Polymerase chain reaction ; Poultry ; Protein kinase C ; Proteins ; Real-Time Polymerase Chain Reaction ; Reverse Transcriptase Polymerase Chain Reaction ; Reverse transcription ; RNA, Small Interfering - genetics ; Secretion ; Signal transduction ; Signal Transduction - drug effects ; siRNA ; Strychnine - analogs & derivatives ; Strychnine - pharmacology ; TOR protein ; Tumors ; Vascular endothelial growth factor ; Vascular Endothelial Growth Factor Receptor-2 - antagonists & inhibitors ; Vascular Endothelial Growth Factor Receptor-2 - genetics ; Vascular Endothelial Growth Factor Receptor-2 - metabolism ; Viability</subject><ispartof>Journal of cellular and molecular medicine, 2013-10, Vol.17 (10), p.1316-1324</ispartof><rights>2013 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine</rights><rights>2013 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.</rights><rights>2013. This work is published under http://creativecommons.org/licenses/by/3.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2013 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine 2013</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4488-c9a29622dc6681edefb4edef34b200a5c91d75726be1fc774b53aef058b04b053</citedby><cites>FETCH-LOGICAL-c4488-c9a29622dc6681edefb4edef34b200a5c91d75726be1fc774b53aef058b04b053</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/PMC4159018/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4159018/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,1411,11542,27903,27904,45553,45554,46030,46454,53769,53771</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23905676$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Luo, Wenjuan</creatorcontrib><creatorcontrib>Wang, Xiaoli</creatorcontrib><creatorcontrib>Zheng, Lei</creatorcontrib><creatorcontrib>Zhan, Yingzhuan</creatorcontrib><creatorcontrib>Zhang, Dongdong</creatorcontrib><creatorcontrib>Zhang, Jie</creatorcontrib><creatorcontrib>Zhang, Yanmin</creatorcontrib><title>Brucine suppresses colon cancer cells growth via mediating KDR signalling pathway</title><title>Journal of cellular and molecular medicine</title><addtitle>J Cell Mol Med</addtitle><description>Angiogenesis plays an important role in colon cancer development. This study aimed to demonstrate the effect of brucine on tumour angiogenesis and its mechanism of action. The anti‐angiogenic effect was evaluated on the chicken chorioallantoic membrane (CAM) model and tube formation. The mechanism was demonstrated through detecting mRNA and protein expressions of VEGFR2 (KDR), PKCα, PLCγ and Raf1 by reverse transcription‐polymerase chain reaction (RT‐PCR) and Western blot (WB), as well as expressions of VEGF and PKCβ and mTOR by ELISA and WB. The results showed that brucine significantly reduced angiogenesis of CAM and tube formation, inhibited the VEGF secretion and mTOR expression in LoVo cell and down‐regulated the mRNA and phosphorylation protein expressions of KDR, PKCα, PLCγ and Raf1. In addition, the effects of brucine on KDR kinase activity, viability of LoVo cell and gene knockdown cell were detected with the Lance™ assay, WST‐1 assay and instantaneous siRNA. Compared to that of normal LoVo cells, the inhibition on proliferation of knockdown cells by brucine decreased significantly. These results suggest that brucine could inhibit angiogenesis and be a useful therapeutic candidate for colon cancer intervention.</description><subject>Angiogenesis</subject><subject>Apoptosis</subject><subject>Base Sequence</subject><subject>Brucine</subject><subject>Cell adhesion & migration</subject><subject>Cell Division - drug effects</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell proliferation</subject><subject>Chorioallantoic membrane</subject><subject>Colon cancer</subject><subject>Colonic Neoplasms - metabolism</subject><subject>Colonic Neoplasms - pathology</subject><subject>Colorectal cancer</subject><subject>DNA Primers</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Humans</subject><subject>KDR</subject><subject>Kinases</subject><subject>LoVo cells</subject><subject>Original</subject><subject>Phosphorylation</subject><subject>Polymerase chain reaction</subject><subject>Poultry</subject><subject>Protein kinase C</subject><subject>Proteins</subject><subject>Real-Time Polymerase Chain Reaction</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>Reverse transcription</subject><subject>RNA, Small Interfering - genetics</subject><subject>Secretion</subject><subject>Signal transduction</subject><subject>Signal Transduction - drug effects</subject><subject>siRNA</subject><subject>Strychnine - analogs & derivatives</subject><subject>Strychnine - pharmacology</subject><subject>TOR protein</subject><subject>Tumors</subject><subject>Vascular endothelial growth factor</subject><subject>Vascular Endothelial Growth Factor Receptor-2 - antagonists & inhibitors</subject><subject>Vascular Endothelial Growth Factor Receptor-2 - genetics</subject><subject>Vascular Endothelial Growth Factor Receptor-2 - metabolism</subject><subject>Viability</subject><issn>1582-1838</issn><issn>1582-4934</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>24P</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>eNp9kE9PwyAYh4nROJ1e_ACGxJtJJ1BK4WKi879bjEbPhDK6sXRthXbLvr2tnYte5PDCG578eHkAOMFogJt1MdeLxQATjPgOOMARJwEVId3dnDEPeQ8cej9HKGQ4FPugR0KBIhazA_B67WptcwN9XZbOeG881EVW5FCrXBsHtckyD6euWFUzuLQKLszEqsrmU_h88wa9neYqy9q2VNVspdZHYC9VmTfHm70PPu5u34cPwejl_nF4NQo0pZwHWigiGCETzRjHZmLShLY1pAlBSEVa4EkcxYQlBqc6jmkShcqkKOIJogmKwj647HLLOmlm0iavnMpk6exCubUslJV_b3I7k9NiKSmOBGqs9MHZJsAVn7XxlZwXtWt-4yUhQmDGGWENdd5R2hXeO5NuX8BItvplq19-62_g098zbdEf3w2AO2BlM7P-J0o-DcfjLvQLsLKRzg</recordid><startdate>201310</startdate><enddate>201310</enddate><creator>Luo, Wenjuan</creator><creator>Wang, Xiaoli</creator><creator>Zheng, Lei</creator><creator>Zhan, Yingzhuan</creator><creator>Zhang, Dongdong</creator><creator>Zhang, Jie</creator><creator>Zhang, Yanmin</creator><general>John Wiley & Sons, Inc</general><general>Blackwell Publishing Ltd</general><scope>24P</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>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>5PM</scope></search><sort><creationdate>201310</creationdate><title>Brucine suppresses colon cancer cells growth via mediating KDR signalling pathway</title><author>Luo, Wenjuan ; Wang, Xiaoli ; Zheng, Lei ; Zhan, Yingzhuan ; Zhang, Dongdong ; Zhang, Jie ; Zhang, Yanmin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4488-c9a29622dc6681edefb4edef34b200a5c91d75726be1fc774b53aef058b04b053</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Angiogenesis</topic><topic>Apoptosis</topic><topic>Base Sequence</topic><topic>Brucine</topic><topic>Cell adhesion & migration</topic><topic>Cell Division - drug effects</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell proliferation</topic><topic>Chorioallantoic membrane</topic><topic>Colon cancer</topic><topic>Colonic Neoplasms - metabolism</topic><topic>Colonic Neoplasms - pathology</topic><topic>Colorectal cancer</topic><topic>DNA Primers</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Humans</topic><topic>KDR</topic><topic>Kinases</topic><topic>LoVo cells</topic><topic>Original</topic><topic>Phosphorylation</topic><topic>Polymerase chain reaction</topic><topic>Poultry</topic><topic>Protein kinase C</topic><topic>Proteins</topic><topic>Real-Time Polymerase Chain Reaction</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>Reverse transcription</topic><topic>RNA, Small Interfering - genetics</topic><topic>Secretion</topic><topic>Signal transduction</topic><topic>Signal Transduction - drug effects</topic><topic>siRNA</topic><topic>Strychnine - analogs & derivatives</topic><topic>Strychnine - pharmacology</topic><topic>TOR protein</topic><topic>Tumors</topic><topic>Vascular endothelial growth factor</topic><topic>Vascular Endothelial Growth Factor Receptor-2 - antagonists & inhibitors</topic><topic>Vascular Endothelial Growth Factor Receptor-2 - genetics</topic><topic>Vascular Endothelial Growth Factor Receptor-2 - metabolism</topic><topic>Viability</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Luo, Wenjuan</creatorcontrib><creatorcontrib>Wang, Xiaoli</creatorcontrib><creatorcontrib>Zheng, Lei</creatorcontrib><creatorcontrib>Zhan, Yingzhuan</creatorcontrib><creatorcontrib>Zhang, Dongdong</creatorcontrib><creatorcontrib>Zhang, Jie</creatorcontrib><creatorcontrib>Zhang, Yanmin</creatorcontrib><collection>Wiley Online Library Open Access</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>ProQuest Health and Medical</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>ProQuest Science Journals</collection><collection>ProQuest Biological Science Journals</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 China</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</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>Luo, Wenjuan</au><au>Wang, Xiaoli</au><au>Zheng, Lei</au><au>Zhan, Yingzhuan</au><au>Zhang, Dongdong</au><au>Zhang, Jie</au><au>Zhang, Yanmin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Brucine suppresses colon cancer cells growth via mediating KDR signalling pathway</atitle><jtitle>Journal of cellular and molecular medicine</jtitle><addtitle>J Cell Mol Med</addtitle><date>2013-10</date><risdate>2013</risdate><volume>17</volume><issue>10</issue><spage>1316</spage><epage>1324</epage><pages>1316-1324</pages><issn>1582-1838</issn><eissn>1582-4934</eissn><abstract>Angiogenesis plays an important role in colon cancer development. This study aimed to demonstrate the effect of brucine on tumour angiogenesis and its mechanism of action. The anti‐angiogenic effect was evaluated on the chicken chorioallantoic membrane (CAM) model and tube formation. The mechanism was demonstrated through detecting mRNA and protein expressions of VEGFR2 (KDR), PKCα, PLCγ and Raf1 by reverse transcription‐polymerase chain reaction (RT‐PCR) and Western blot (WB), as well as expressions of VEGF and PKCβ and mTOR by ELISA and WB. The results showed that brucine significantly reduced angiogenesis of CAM and tube formation, inhibited the VEGF secretion and mTOR expression in LoVo cell and down‐regulated the mRNA and phosphorylation protein expressions of KDR, PKCα, PLCγ and Raf1. In addition, the effects of brucine on KDR kinase activity, viability of LoVo cell and gene knockdown cell were detected with the Lance™ assay, WST‐1 assay and instantaneous siRNA. Compared to that of normal LoVo cells, the inhibition on proliferation of knockdown cells by brucine decreased significantly. These results suggest that brucine could inhibit angiogenesis and be a useful therapeutic candidate for colon cancer intervention.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>23905676</pmid><doi>10.1111/jcmm.12108</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Angiogenesis Apoptosis Base Sequence Brucine Cell adhesion & migration Cell Division - drug effects Cell growth Cell Line, Tumor Cell proliferation Chorioallantoic membrane Colon cancer Colonic Neoplasms - metabolism Colonic Neoplasms - pathology Colorectal cancer DNA Primers Enzyme-linked immunosorbent assay Humans KDR Kinases LoVo cells Original Phosphorylation Polymerase chain reaction Poultry Protein kinase C Proteins Real-Time Polymerase Chain Reaction Reverse Transcriptase Polymerase Chain Reaction Reverse transcription RNA, Small Interfering - genetics Secretion Signal transduction Signal Transduction - drug effects siRNA Strychnine - analogs & derivatives Strychnine - pharmacology TOR protein Tumors Vascular endothelial growth factor Vascular Endothelial Growth Factor Receptor-2 - antagonists & inhibitors Vascular Endothelial Growth Factor Receptor-2 - genetics Vascular Endothelial Growth Factor Receptor-2 - metabolism Viability |
| title | Brucine suppresses colon cancer cells growth via mediating KDR signalling pathway |
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