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Glioma stem cells-derived exosomal miR-26a promotes angiogenesis of microvessel endothelial cells in glioma
Cancer stem cells (CSCs), which are involved in cancer initiation and metastasis, could potentially release exosomes that mediate cellular communication by delivering microRNAs (miRNAs). Based on the role of miR-26a in angiogenesis of glioma, our study was performed to investigate whether glioma ste...
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| Published in: | Journal of experimental & clinical cancer research 2019-05, Vol.38 (1), p.201-201, Article 201 |
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| creator | Wang, Zhi-Fei Liao, Fan Wu, Hao Dai, Jin |
| description | Cancer stem cells (CSCs), which are involved in cancer initiation and metastasis, could potentially release exosomes that mediate cellular communication by delivering microRNAs (miRNAs). Based on the role of miR-26a in angiogenesis of glioma, our study was performed to investigate whether glioma stem cells (GSCs)-derived exosomes containing miR-26a could exert effects on angiogenesis of microvessel endothelial cells in glioma, in order to provide a new therapeutic RNA vehicle for glioma therapies.
The expression of miR-26a and PTEN in glioma was quantified and the interaction among miR-26a, PTEN and PI3K/Akt signaling pathway was examined. Next, a series of gain- and loss-of function experiments were conducted to determine the role of miR-26a in angiogenesis of human brain microvascular endothelial cells (HBMECs). Subsequently, HBMECs were exposed to exosomes derived from GSCs with the gain-/loss-of-function of miR-26a. Finally, the effect of exosomal miR-26a on angiogenesis of HBMECs was assessed both in vitro and in vivo.
The results revealed that PTEN was down-regulated, while miR-26a was up-regulated in glioma. miR-26a activated the PI3K/Akt signaling pathway by targeting PTEN. Restored miR-26a promoted proliferation, migration, tube formation, and angiogenesis of HBMECs in vitro. In addition, GSCs-derived exosomes overexpressing miR-26a contributed to enhanced proliferation and angiogenesis of HBMECs in vitro through inhibition of PTEN. The angiogenic effects of GSCs-derived exosomes overexpressing miR-26a in vivo were consistent with the above-mentioned in vitro findings.
Collectively, our study demonstrates that GSCs-derived exosomal miR-26a promotes angiogenesis of HBMECs, highlighting an angiogenic role of miR-26a via exosomes. |
| doi_str_mv | 10.1186/s13046-019-1181-4 |
| format | article |
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The expression of miR-26a and PTEN in glioma was quantified and the interaction among miR-26a, PTEN and PI3K/Akt signaling pathway was examined. Next, a series of gain- and loss-of function experiments were conducted to determine the role of miR-26a in angiogenesis of human brain microvascular endothelial cells (HBMECs). Subsequently, HBMECs were exposed to exosomes derived from GSCs with the gain-/loss-of-function of miR-26a. Finally, the effect of exosomal miR-26a on angiogenesis of HBMECs was assessed both in vitro and in vivo.
The results revealed that PTEN was down-regulated, while miR-26a was up-regulated in glioma. miR-26a activated the PI3K/Akt signaling pathway by targeting PTEN. Restored miR-26a promoted proliferation, migration, tube formation, and angiogenesis of HBMECs in vitro. In addition, GSCs-derived exosomes overexpressing miR-26a contributed to enhanced proliferation and angiogenesis of HBMECs in vitro through inhibition of PTEN. The angiogenic effects of GSCs-derived exosomes overexpressing miR-26a in vivo were consistent with the above-mentioned in vitro findings.
Collectively, our study demonstrates that GSCs-derived exosomal miR-26a promotes angiogenesis of HBMECs, highlighting an angiogenic role of miR-26a via exosomes.</description><identifier>ISSN: 1756-9966</identifier><identifier>ISSN: 0392-9078</identifier><identifier>EISSN: 1756-9966</identifier><identifier>DOI: 10.1186/s13046-019-1181-4</identifier><identifier>PMID: 31101062</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Adult ; Aged ; Angiogenesis ; Animals ; Biomarkers ; Brain ; Brain cancer ; Brain research ; Cancer ; Cancer metastasis ; Cancer therapies ; Care and treatment ; Cell growth ; Cell Movement - genetics ; Cell Proliferation - genetics ; Cellular signal transduction ; Coculture Techniques ; Endothelial Cells - metabolism ; Endothelial Cells - pathology ; Endothelium ; Exosomes ; Exosomes - genetics ; Exosomes - pathology ; Female ; Gene expression ; Gene Expression Regulation, Neoplastic - genetics ; Genetic aspects ; Glioma ; Glioma - genetics ; Glioma - pathology ; Glioma stem cells ; Gliomas ; Heterografts ; Humans ; Laboratory animals ; Male ; Medical prognosis ; Mice ; MicroRNA ; microRNA-26a ; MicroRNAs - genetics ; Microvessel endothelial cells ; Microvessels - metabolism ; Microvessels - pathology ; Middle Aged ; Neoplastic Stem Cells - metabolism ; Neoplastic Stem Cells - pathology ; Neovascularization ; Phosphatase and tensin homolog deleted on chromosome ten ; Phosphatases ; Phosphatidylinositol 3-Kinases - genetics ; Prognosis ; Prostate cancer ; Proto-Oncogene Proteins c-akt - genetics ; PTEN Phosphohydrolase - genetics ; Risk factors ; RNA ; Signal Transduction - genetics ; Stem cell transplantation ; Stem cells ; Tumors</subject><ispartof>Journal of experimental & clinical cancer research, 2019-05, Vol.38 (1), p.201-201, Article 201</ispartof><rights>COPYRIGHT 2019 BioMed Central Ltd.</rights><rights>2019. This work is licensed 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>The Author(s). 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c591t-cc1995ccf65347241e32b6dff47044493a1caf37ac61b9a7e8d0bc65ca0753303</citedby><cites>FETCH-LOGICAL-c591t-cc1995ccf65347241e32b6dff47044493a1caf37ac61b9a7e8d0bc65ca0753303</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/PMC6525364/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2227039821?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31101062$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Zhi-Fei</creatorcontrib><creatorcontrib>Liao, Fan</creatorcontrib><creatorcontrib>Wu, Hao</creatorcontrib><creatorcontrib>Dai, Jin</creatorcontrib><title>Glioma stem cells-derived exosomal miR-26a promotes angiogenesis of microvessel endothelial cells in glioma</title><title>Journal of experimental & clinical cancer research</title><addtitle>J Exp Clin Cancer Res</addtitle><description>Cancer stem cells (CSCs), which are involved in cancer initiation and metastasis, could potentially release exosomes that mediate cellular communication by delivering microRNAs (miRNAs). Based on the role of miR-26a in angiogenesis of glioma, our study was performed to investigate whether glioma stem cells (GSCs)-derived exosomes containing miR-26a could exert effects on angiogenesis of microvessel endothelial cells in glioma, in order to provide a new therapeutic RNA vehicle for glioma therapies.
The expression of miR-26a and PTEN in glioma was quantified and the interaction among miR-26a, PTEN and PI3K/Akt signaling pathway was examined. Next, a series of gain- and loss-of function experiments were conducted to determine the role of miR-26a in angiogenesis of human brain microvascular endothelial cells (HBMECs). Subsequently, HBMECs were exposed to exosomes derived from GSCs with the gain-/loss-of-function of miR-26a. Finally, the effect of exosomal miR-26a on angiogenesis of HBMECs was assessed both in vitro and in vivo.
The results revealed that PTEN was down-regulated, while miR-26a was up-regulated in glioma. miR-26a activated the PI3K/Akt signaling pathway by targeting PTEN. Restored miR-26a promoted proliferation, migration, tube formation, and angiogenesis of HBMECs in vitro. In addition, GSCs-derived exosomes overexpressing miR-26a contributed to enhanced proliferation and angiogenesis of HBMECs in vitro through inhibition of PTEN. The angiogenic effects of GSCs-derived exosomes overexpressing miR-26a in vivo were consistent with the above-mentioned in vitro findings.
Collectively, our study demonstrates that GSCs-derived exosomal miR-26a promotes angiogenesis of HBMECs, highlighting an angiogenic role of miR-26a via exosomes.</description><subject>Adult</subject><subject>Aged</subject><subject>Angiogenesis</subject><subject>Animals</subject><subject>Biomarkers</subject><subject>Brain</subject><subject>Brain cancer</subject><subject>Brain research</subject><subject>Cancer</subject><subject>Cancer metastasis</subject><subject>Cancer therapies</subject><subject>Care and treatment</subject><subject>Cell growth</subject><subject>Cell Movement - genetics</subject><subject>Cell Proliferation - genetics</subject><subject>Cellular signal transduction</subject><subject>Coculture Techniques</subject><subject>Endothelial Cells - metabolism</subject><subject>Endothelial Cells - pathology</subject><subject>Endothelium</subject><subject>Exosomes</subject><subject>Exosomes - genetics</subject><subject>Exosomes - pathology</subject><subject>Female</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic - genetics</subject><subject>Genetic aspects</subject><subject>Glioma</subject><subject>Glioma - genetics</subject><subject>Glioma - pathology</subject><subject>Glioma stem cells</subject><subject>Gliomas</subject><subject>Heterografts</subject><subject>Humans</subject><subject>Laboratory animals</subject><subject>Male</subject><subject>Medical prognosis</subject><subject>Mice</subject><subject>MicroRNA</subject><subject>microRNA-26a</subject><subject>MicroRNAs - genetics</subject><subject>Microvessel endothelial cells</subject><subject>Microvessels - metabolism</subject><subject>Microvessels - pathology</subject><subject>Middle Aged</subject><subject>Neoplastic Stem Cells - metabolism</subject><subject>Neoplastic Stem Cells - pathology</subject><subject>Neovascularization</subject><subject>Phosphatase and tensin homolog deleted on chromosome ten</subject><subject>Phosphatases</subject><subject>Phosphatidylinositol 3-Kinases - genetics</subject><subject>Prognosis</subject><subject>Prostate cancer</subject><subject>Proto-Oncogene Proteins c-akt - genetics</subject><subject>PTEN Phosphohydrolase - genetics</subject><subject>Risk factors</subject><subject>RNA</subject><subject>Signal Transduction - genetics</subject><subject>Stem cell transplantation</subject><subject>Stem cells</subject><subject>Tumors</subject><issn>1756-9966</issn><issn>0392-9078</issn><issn>1756-9966</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNptkk2LFDEQhhtR3HX1B3iRBkG89Jrv7lyEZdF1YUEQPYd0Ut2TMZ2MSc-g_970zLrOiOSQj3rfp0hVVdVLjC4x7sS7jCliokFYNuWOG_aoOsctF42UQjw-Op9Vz3JeIySwxPJpdUYxRhgJcl59v_EuTrrOM0y1Ae9zYyG5HdgafsZcQr6e3JeGCF1vUpziDLnWYXRxhADZ5ToORWBS3EHO4GsINs4r8K4Y97zahXrcJ3lePRm0z_Difr-ovn388PX6U3P3-eb2-uquMVziuTEGS8mNGQSnrCUMAyW9sMPAWsQYk1RjowfaaiNwL3ULnUW9Edxo1HJKEb2obg9cG_VabZKbdPqlonZq_xDTqHSanfGgmG3RwHvd2kLuCfQF2Ft9yN6RrrDeH1ibbT-BNRDmpP0J9DQS3EqNcacEJ5wKVgBv7wEp_thCntXk8lIYHSBusyKEEsRIx0WRvv5Huo7bFEqpioq0iMqO4L-qUZcPuDDEktcsUHXFO8Ex4d2S9vI_qrIslG7FAIMr7yeGN0eGFWg_r3L029nFkE-F-CAsPc85wfBQDIzUMpbqMJaqjOVyx2rxvDqu4oPjzxzS3w013Pk</recordid><startdate>20190517</startdate><enddate>20190517</enddate><creator>Wang, Zhi-Fei</creator><creator>Liao, Fan</creator><creator>Wu, Hao</creator><creator>Dai, Jin</creator><general>BioMed Central Ltd</general><general>BioMed Central</general><general>BMC</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>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20190517</creationdate><title>Glioma stem cells-derived exosomal miR-26a promotes angiogenesis of microvessel endothelial cells in glioma</title><author>Wang, Zhi-Fei ; Liao, Fan ; Wu, Hao ; Dai, Jin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c591t-cc1995ccf65347241e32b6dff47044493a1caf37ac61b9a7e8d0bc65ca0753303</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Angiogenesis</topic><topic>Animals</topic><topic>Biomarkers</topic><topic>Brain</topic><topic>Brain cancer</topic><topic>Brain research</topic><topic>Cancer</topic><topic>Cancer metastasis</topic><topic>Cancer therapies</topic><topic>Care and treatment</topic><topic>Cell growth</topic><topic>Cell Movement - genetics</topic><topic>Cell Proliferation - genetics</topic><topic>Cellular signal transduction</topic><topic>Coculture Techniques</topic><topic>Endothelial Cells - metabolism</topic><topic>Endothelial Cells - pathology</topic><topic>Endothelium</topic><topic>Exosomes</topic><topic>Exosomes - genetics</topic><topic>Exosomes - pathology</topic><topic>Female</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Neoplastic - genetics</topic><topic>Genetic aspects</topic><topic>Glioma</topic><topic>Glioma - genetics</topic><topic>Glioma - pathology</topic><topic>Glioma stem cells</topic><topic>Gliomas</topic><topic>Heterografts</topic><topic>Humans</topic><topic>Laboratory animals</topic><topic>Male</topic><topic>Medical prognosis</topic><topic>Mice</topic><topic>MicroRNA</topic><topic>microRNA-26a</topic><topic>MicroRNAs - genetics</topic><topic>Microvessel endothelial cells</topic><topic>Microvessels - metabolism</topic><topic>Microvessels - pathology</topic><topic>Middle Aged</topic><topic>Neoplastic Stem Cells - metabolism</topic><topic>Neoplastic Stem Cells - pathology</topic><topic>Neovascularization</topic><topic>Phosphatase and tensin homolog deleted on chromosome ten</topic><topic>Phosphatases</topic><topic>Phosphatidylinositol 3-Kinases - genetics</topic><topic>Prognosis</topic><topic>Prostate cancer</topic><topic>Proto-Oncogene Proteins c-akt - genetics</topic><topic>PTEN Phosphohydrolase - genetics</topic><topic>Risk factors</topic><topic>RNA</topic><topic>Signal Transduction - genetics</topic><topic>Stem cell transplantation</topic><topic>Stem cells</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Zhi-Fei</creatorcontrib><creatorcontrib>Liao, Fan</creatorcontrib><creatorcontrib>Wu, Hao</creatorcontrib><creatorcontrib>Dai, Jin</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>ProQuest Health and Medical</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</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)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>ProQuest - 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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>Directory of Open Access Journals</collection><jtitle>Journal of experimental & clinical cancer research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Zhi-Fei</au><au>Liao, Fan</au><au>Wu, Hao</au><au>Dai, Jin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Glioma stem cells-derived exosomal miR-26a promotes angiogenesis of microvessel endothelial cells in glioma</atitle><jtitle>Journal of experimental & clinical cancer research</jtitle><addtitle>J Exp Clin Cancer Res</addtitle><date>2019-05-17</date><risdate>2019</risdate><volume>38</volume><issue>1</issue><spage>201</spage><epage>201</epage><pages>201-201</pages><artnum>201</artnum><issn>1756-9966</issn><issn>0392-9078</issn><eissn>1756-9966</eissn><abstract>Cancer stem cells (CSCs), which are involved in cancer initiation and metastasis, could potentially release exosomes that mediate cellular communication by delivering microRNAs (miRNAs). Based on the role of miR-26a in angiogenesis of glioma, our study was performed to investigate whether glioma stem cells (GSCs)-derived exosomes containing miR-26a could exert effects on angiogenesis of microvessel endothelial cells in glioma, in order to provide a new therapeutic RNA vehicle for glioma therapies.
The expression of miR-26a and PTEN in glioma was quantified and the interaction among miR-26a, PTEN and PI3K/Akt signaling pathway was examined. Next, a series of gain- and loss-of function experiments were conducted to determine the role of miR-26a in angiogenesis of human brain microvascular endothelial cells (HBMECs). Subsequently, HBMECs were exposed to exosomes derived from GSCs with the gain-/loss-of-function of miR-26a. Finally, the effect of exosomal miR-26a on angiogenesis of HBMECs was assessed both in vitro and in vivo.
The results revealed that PTEN was down-regulated, while miR-26a was up-regulated in glioma. miR-26a activated the PI3K/Akt signaling pathway by targeting PTEN. Restored miR-26a promoted proliferation, migration, tube formation, and angiogenesis of HBMECs in vitro. In addition, GSCs-derived exosomes overexpressing miR-26a contributed to enhanced proliferation and angiogenesis of HBMECs in vitro through inhibition of PTEN. The angiogenic effects of GSCs-derived exosomes overexpressing miR-26a in vivo were consistent with the above-mentioned in vitro findings.
Collectively, our study demonstrates that GSCs-derived exosomal miR-26a promotes angiogenesis of HBMECs, highlighting an angiogenic role of miR-26a via exosomes.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>31101062</pmid><doi>10.1186/s13046-019-1181-4</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adult Aged Angiogenesis Animals Biomarkers Brain Brain cancer Brain research Cancer Cancer metastasis Cancer therapies Care and treatment Cell growth Cell Movement - genetics Cell Proliferation - genetics Cellular signal transduction Coculture Techniques Endothelial Cells - metabolism Endothelial Cells - pathology Endothelium Exosomes Exosomes - genetics Exosomes - pathology Female Gene expression Gene Expression Regulation, Neoplastic - genetics Genetic aspects Glioma Glioma - genetics Glioma - pathology Glioma stem cells Gliomas Heterografts Humans Laboratory animals Male Medical prognosis Mice MicroRNA microRNA-26a MicroRNAs - genetics Microvessel endothelial cells Microvessels - metabolism Microvessels - pathology Middle Aged Neoplastic Stem Cells - metabolism Neoplastic Stem Cells - pathology Neovascularization Phosphatase and tensin homolog deleted on chromosome ten Phosphatases Phosphatidylinositol 3-Kinases - genetics Prognosis Prostate cancer Proto-Oncogene Proteins c-akt - genetics PTEN Phosphohydrolase - genetics Risk factors RNA Signal Transduction - genetics Stem cell transplantation Stem cells Tumors |
| title | Glioma stem cells-derived exosomal miR-26a promotes angiogenesis of microvessel endothelial cells in glioma |
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