Melittin Inhibits Hypoxia-Induced Vasculogenic Mimicry Formation and Epithelial-Mesenchymal Transition through Suppression of HIF-1α/Akt Pathway in Liver Cancer
In this study, we investigated whether melittin could suppress hypoxia-induced vasculogenic mimicry (VM) formation in liver cancer and explored the underlying mechanisms. Melittin significantly inhibited the proliferation of liver cancer cells with or without CoCl2 presence. Melittin also significan...
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| Veröffentlicht in: | Evidence-based complementary and alternative medicine 2019-01, Vol.2019 (2019), p.1-10 |
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| creator | Cheng, Binbin Ling, Changquan Shu, Qijin Chen, Peifeng Ruan, Shanming Liang, Shufang Zou, Yong Yin, Zifei Lin, Wanfu Chen, Qunwei Li, Shu |
| description | In this study, we investigated whether melittin could suppress hypoxia-induced vasculogenic mimicry (VM) formation in liver cancer and explored the underlying mechanisms. Melittin significantly inhibited the proliferation of liver cancer cells with or without CoCl2 presence. Melittin also significantly inhibited CoCl2-induced migration, invasion, and VM formation of liver cancer cells. CoCl2 treatment suppressed the expression of E-cadherin and elevated the expression of N-cadherin and Vimentin. Melittin reversed the changes in the protein and mRNA levels of these epithelial-mesenchymal transition (EMT) markers. CoCl2-induced accumulation of HIF-1α increased the level of phosphorylated Akt and upregulated the expression of VEGF and MMP-2/9. Melittin decreased the HIF-1α level and thereby suppressed the levels of p-Akt, VEGF, and MMP-2/9. In addition, the inhibitor of PI3K/Akt also suppressed CoCl2-induced EMT and liver cancer cells migration, and the activator of Akt, SC-79, partly blocked the effect of melittin on CoCl2-induced EMT and liver cancer cells migration. In the xenograft tumor model in nude mice, melittin treatment significantly suppressed the tumor growth, VM formation, and HIF-1α expression in the tumor. In conclusion, this study indicates melittin may inhibit hypoxia-induced VM formation and EMT in liver cancer through inhibiting HIF-1α/Akt pathway. |
| doi_str_mv | 10.1155/2019/9602935 |
| format | Article |
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Melittin significantly inhibited the proliferation of liver cancer cells with or without CoCl2 presence. Melittin also significantly inhibited CoCl2-induced migration, invasion, and VM formation of liver cancer cells. CoCl2 treatment suppressed the expression of E-cadherin and elevated the expression of N-cadherin and Vimentin. Melittin reversed the changes in the protein and mRNA levels of these epithelial-mesenchymal transition (EMT) markers. CoCl2-induced accumulation of HIF-1α increased the level of phosphorylated Akt and upregulated the expression of VEGF and MMP-2/9. Melittin decreased the HIF-1α level and thereby suppressed the levels of p-Akt, VEGF, and MMP-2/9. In addition, the inhibitor of PI3K/Akt also suppressed CoCl2-induced EMT and liver cancer cells migration, and the activator of Akt, SC-79, partly blocked the effect of melittin on CoCl2-induced EMT and liver cancer cells migration. In the xenograft tumor model in nude mice, melittin treatment significantly suppressed the tumor growth, VM formation, and HIF-1α expression in the tumor. In conclusion, this study indicates melittin may inhibit hypoxia-induced VM formation and EMT in liver cancer through inhibiting HIF-1α/Akt pathway.</description><identifier>ISSN: 1741-427X</identifier><identifier>EISSN: 1741-4288</identifier><identifier>DOI: 10.1155/2019/9602935</identifier><identifier>PMID: 31057657</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>1-Phosphatidylinositol 3-kinase ; AKT protein ; Angiogenesis ; Biochemistry ; Biology ; Cell adhesion & migration ; Cell growth ; Cell migration ; Cell proliferation ; E-cadherin ; Evidence-based medicine ; Gelatinase A ; Hepatocytes ; Hypoxia ; Liver ; Liver cancer ; Medical prognosis ; Mesenchyme ; Metastasis ; Mimicry ; mRNA ; N-Cadherin ; Tumors ; Vascular endothelial growth factor ; Vimentin ; Xenografts</subject><ispartof>Evidence-based complementary and alternative medicine, 2019-01, Vol.2019 (2019), p.1-10</ispartof><rights>Copyright © 2019 Qunwei Chen et al.</rights><rights>Copyright © 2019 Qunwei Chen et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. https://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2019 Qunwei Chen et al. 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c433t-67e1fe0471758b696cb644fd3d1287ff71cfe79f2d3357443160630af37463da3</citedby><cites>FETCH-LOGICAL-c433t-67e1fe0471758b696cb644fd3d1287ff71cfe79f2d3357443160630af37463da3</cites><orcidid>0000-0001-8435-7952 ; 0000-0002-0037-4059 ; 0000-0003-2483-3392 ; 0000-0002-1914-6689 ; 0000-0002-3338-3269 ; 0000-0003-1061-5255 ; 0000-0002-6362-2945 ; 0000-0002-8321-130X ; 0000-0002-4371-2783</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6463627/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6463627/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,725,778,782,883,27907,27908,53774,53776</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31057657$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Du, Caigan</contributor><contributor>Caigan Du</contributor><creatorcontrib>Cheng, Binbin</creatorcontrib><creatorcontrib>Ling, Changquan</creatorcontrib><creatorcontrib>Shu, Qijin</creatorcontrib><creatorcontrib>Chen, Peifeng</creatorcontrib><creatorcontrib>Ruan, Shanming</creatorcontrib><creatorcontrib>Liang, Shufang</creatorcontrib><creatorcontrib>Zou, Yong</creatorcontrib><creatorcontrib>Yin, Zifei</creatorcontrib><creatorcontrib>Lin, Wanfu</creatorcontrib><creatorcontrib>Chen, Qunwei</creatorcontrib><creatorcontrib>Li, Shu</creatorcontrib><title>Melittin Inhibits Hypoxia-Induced Vasculogenic Mimicry Formation and Epithelial-Mesenchymal Transition through Suppression of HIF-1α/Akt Pathway in Liver Cancer</title><title>Evidence-based complementary and alternative medicine</title><addtitle>Evid Based Complement Alternat Med</addtitle><description>In this study, we investigated whether melittin could suppress hypoxia-induced vasculogenic mimicry (VM) formation in liver cancer and explored the underlying mechanisms. Melittin significantly inhibited the proliferation of liver cancer cells with or without CoCl2 presence. Melittin also significantly inhibited CoCl2-induced migration, invasion, and VM formation of liver cancer cells. CoCl2 treatment suppressed the expression of E-cadherin and elevated the expression of N-cadherin and Vimentin. Melittin reversed the changes in the protein and mRNA levels of these epithelial-mesenchymal transition (EMT) markers. CoCl2-induced accumulation of HIF-1α increased the level of phosphorylated Akt and upregulated the expression of VEGF and MMP-2/9. Melittin decreased the HIF-1α level and thereby suppressed the levels of p-Akt, VEGF, and MMP-2/9. In addition, the inhibitor of PI3K/Akt also suppressed CoCl2-induced EMT and liver cancer cells migration, and the activator of Akt, SC-79, partly blocked the effect of melittin on CoCl2-induced EMT and liver cancer cells migration. In the xenograft tumor model in nude mice, melittin treatment significantly suppressed the tumor growth, VM formation, and HIF-1α expression in the tumor. In conclusion, this study indicates melittin may inhibit hypoxia-induced VM formation and EMT in liver cancer through inhibiting HIF-1α/Akt pathway.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>AKT protein</subject><subject>Angiogenesis</subject><subject>Biochemistry</subject><subject>Biology</subject><subject>Cell adhesion & migration</subject><subject>Cell growth</subject><subject>Cell migration</subject><subject>Cell proliferation</subject><subject>E-cadherin</subject><subject>Evidence-based medicine</subject><subject>Gelatinase A</subject><subject>Hepatocytes</subject><subject>Hypoxia</subject><subject>Liver</subject><subject>Liver cancer</subject><subject>Medical prognosis</subject><subject>Mesenchyme</subject><subject>Metastasis</subject><subject>Mimicry</subject><subject>mRNA</subject><subject>N-Cadherin</subject><subject>Tumors</subject><subject>Vascular endothelial growth factor</subject><subject>Vimentin</subject><subject>Xenografts</subject><issn>1741-427X</issn><issn>1741-4288</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqN0cuO0zAUBuAIgZihsGONLLFBglA7viUbpFE1pZVagcSA2EWuYzceEjvYzgx9HB6BF-GZcGkplxUrW_bn3-foZNljBF8iROm0gKiaVgwWFaZ3snPECcpJUZZ3T3v-8Sx7EMI1TIZzfj87wwhSzig_z76uVWdiNBYsbWs2Jgaw2A3uixH50jajVA34IIIcO7dV1kiwNr2RfgfmzvciGmeBsA24HExsU5Do8rUKysp214sOXHlhg_mpYuvduG3Bu3EYvAphf-Y0WCznOfr-bXrxKYK3Ira3YgdSLStzozyYCSuVf5jd06IL6tFxnWTv55dXs0W-evN6ObtY5ZJgHHPGFdIKEo44LTesYnLDCNENblBRcq05klrxShcNxpQTghGDDEOhMScMNwJPsleH3GHc9KqRykYvunrwphd-Vzth6r9vrGnrrbupWXrPCp4Cnh0DvPs8qhDr3gSpuk5Y5cZQFwVGFSxI-naSPf2HXrvR29ReUrCiCHJWJvXioKR3IXilT8UgWO9nX-9nXx9nn_iTPxs44V_DTuD5AbTGNuLW_GecSkZp8VsjikpI8Q90IMOi</recordid><startdate>20190101</startdate><enddate>20190101</enddate><creator>Cheng, 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Inhibits Hypoxia-Induced Vasculogenic Mimicry Formation and Epithelial-Mesenchymal Transition through Suppression of HIF-1α/Akt Pathway in Liver Cancer</title><author>Cheng, Binbin ; Ling, Changquan ; Shu, Qijin ; Chen, Peifeng ; Ruan, Shanming ; Liang, Shufang ; Zou, Yong ; Yin, Zifei ; Lin, Wanfu ; Chen, Qunwei ; Li, Shu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c433t-67e1fe0471758b696cb644fd3d1287ff71cfe79f2d3357443160630af37463da3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>AKT protein</topic><topic>Angiogenesis</topic><topic>Biochemistry</topic><topic>Biology</topic><topic>Cell adhesion & migration</topic><topic>Cell growth</topic><topic>Cell migration</topic><topic>Cell proliferation</topic><topic>E-cadherin</topic><topic>Evidence-based medicine</topic><topic>Gelatinase A</topic><topic>Hepatocytes</topic><topic>Hypoxia</topic><topic>Liver</topic><topic>Liver cancer</topic><topic>Medical prognosis</topic><topic>Mesenchyme</topic><topic>Metastasis</topic><topic>Mimicry</topic><topic>mRNA</topic><topic>N-Cadherin</topic><topic>Tumors</topic><topic>Vascular endothelial growth factor</topic><topic>Vimentin</topic><topic>Xenografts</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cheng, Binbin</creatorcontrib><creatorcontrib>Ling, Changquan</creatorcontrib><creatorcontrib>Shu, Qijin</creatorcontrib><creatorcontrib>Chen, Peifeng</creatorcontrib><creatorcontrib>Ruan, Shanming</creatorcontrib><creatorcontrib>Liang, Shufang</creatorcontrib><creatorcontrib>Zou, Yong</creatorcontrib><creatorcontrib>Yin, Zifei</creatorcontrib><creatorcontrib>Lin, Wanfu</creatorcontrib><creatorcontrib>Chen, Qunwei</creatorcontrib><creatorcontrib>Li, Shu</creatorcontrib><collection>الدوريات العلمية والإحصائية - e-Marefa Academic and 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Caigan</au><au>Caigan Du</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Melittin Inhibits Hypoxia-Induced Vasculogenic Mimicry Formation and Epithelial-Mesenchymal Transition through Suppression of HIF-1α/Akt Pathway in Liver Cancer</atitle><jtitle>Evidence-based complementary and alternative medicine</jtitle><addtitle>Evid Based Complement Alternat Med</addtitle><date>2019-01-01</date><risdate>2019</risdate><volume>2019</volume><issue>2019</issue><spage>1</spage><epage>10</epage><pages>1-10</pages><issn>1741-427X</issn><eissn>1741-4288</eissn><abstract>In this study, we investigated whether melittin could suppress hypoxia-induced vasculogenic mimicry (VM) formation in liver cancer and explored the underlying mechanisms. Melittin significantly inhibited the proliferation of liver cancer cells with or without CoCl2 presence. Melittin also significantly inhibited CoCl2-induced migration, invasion, and VM formation of liver cancer cells. CoCl2 treatment suppressed the expression of E-cadherin and elevated the expression of N-cadherin and Vimentin. Melittin reversed the changes in the protein and mRNA levels of these epithelial-mesenchymal transition (EMT) markers. CoCl2-induced accumulation of HIF-1α increased the level of phosphorylated Akt and upregulated the expression of VEGF and MMP-2/9. Melittin decreased the HIF-1α level and thereby suppressed the levels of p-Akt, VEGF, and MMP-2/9. In addition, the inhibitor of PI3K/Akt also suppressed CoCl2-induced EMT and liver cancer cells migration, and the activator of Akt, SC-79, partly blocked the effect of melittin on CoCl2-induced EMT and liver cancer cells migration. In the xenograft tumor model in nude mice, melittin treatment significantly suppressed the tumor growth, VM formation, and HIF-1α expression in the tumor. In conclusion, this study indicates melittin may inhibit hypoxia-induced VM formation and EMT in liver cancer through inhibiting HIF-1α/Akt pathway.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>31057657</pmid><doi>10.1155/2019/9602935</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0001-8435-7952</orcidid><orcidid>https://orcid.org/0000-0002-0037-4059</orcidid><orcidid>https://orcid.org/0000-0003-2483-3392</orcidid><orcidid>https://orcid.org/0000-0002-1914-6689</orcidid><orcidid>https://orcid.org/0000-0002-3338-3269</orcidid><orcidid>https://orcid.org/0000-0003-1061-5255</orcidid><orcidid>https://orcid.org/0000-0002-6362-2945</orcidid><orcidid>https://orcid.org/0000-0002-8321-130X</orcidid><orcidid>https://orcid.org/0000-0002-4371-2783</orcidid><oa>free_for_read</oa></addata></record> |
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| source | Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central Open Access; Wiley Online Library Open Access; PubMed Central; Alma/SFX Local Collection |
| subjects | 1-Phosphatidylinositol 3-kinase AKT protein Angiogenesis Biochemistry Biology Cell adhesion & migration Cell growth Cell migration Cell proliferation E-cadherin Evidence-based medicine Gelatinase A Hepatocytes Hypoxia Liver Liver cancer Medical prognosis Mesenchyme Metastasis Mimicry mRNA N-Cadherin Tumors Vascular endothelial growth factor Vimentin Xenografts |
| title | Melittin Inhibits Hypoxia-Induced Vasculogenic Mimicry Formation and Epithelial-Mesenchymal Transition through Suppression of HIF-1α/Akt Pathway in Liver Cancer |
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