Long Non-Coding RNA HOXA-AS2 Regulates Malignant Glioma Behaviors and Vasculogenic Mimicry Formation via the MiR-373/EGFR Axis
Vasculogenic mimicry (VM) has been reported to be a novel glioma neovascularization process. Anti-VM therapy provides new insight into glioma clinical management. In this study, we revealed the role of the long non-coding RNA HOXA cluster antisense RNA 2 (HOXA-AS2) in malignant glioma behaviors and...
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| Veröffentlicht in: | Cellular physiology and biochemistry 2018-01, Vol.45 (1), p.131-147 |
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| creator | Gao, Yana Yu, Hai Liu, Yunhui Liu, Xiaobai Zheng, Jian Ma, Jun Gong, Wei Chen, Jiajia Zhao, Lini Tian, Yu Xue, Yixue |
| description | Vasculogenic mimicry (VM) has been reported to be a novel glioma neovascularization process. Anti-VM therapy provides new insight into glioma clinical management. In this study, we revealed the role of the long non-coding RNA HOXA cluster antisense RNA 2 (HOXA-AS2) in malignant glioma behaviors and VM formation.
Quantitative real-time PCR was performed to determine the expression levels of HOXA-AS2 in glioma samples and glioblastoma cell lines. CD34-periodic acid-Schiff dual-staining was performed to assess VM in glioma samples. CCK-8, transwell, and Matrigel tube formation assays were performed to measure the effects of HOXA-AS2 knockdown on cell viability, migration, invasion, and VM tube formation, respectively. RNA immunoprecipitation, dual-luciferase reporter and Western blot assays were performed to explore the molecular mechanisms underlying the functions of HOXS-AS2 in glioblastoma cells. A nude mouse xenograft model was used to investigate the role of HOXA-AS2 in xenograft glioma growth and VM density. Student's t-tests, one-way ANOVAs followed by Bonferroni posthoc tests, and chi-square tests were used for the statistical analyses.
HOXA-AS2 was upregulated in glioma samples and cell lines and was positively correlated with VM. HOXA-AS2 knockdown attenuated cell viability, migration, invasion, and VM formation in glioma cells and inhibited the expression of vascular endothelial-cadherin (VE-cadherin), as well as the expression and activity of matrix metalloproteinase matrix metalloproteinase (MMP)-2 and MMP-9. miR-373 was downregulated in glioma samples and cell lines and suppressed malignancy in glioblastoma cells. HOXA-AS2 bound to miR-373 and negatively regulated its expression. Epidermal growth factor receptor (EGFR), a target of miR-373, increased the expression levels of VE-cadherin, as well as the expression and activity levels of MMP-2 and MMP-9, via activating phosphatidylinositol 3-kinase/serine/threonine kinase pathways. HOXA-AS2 knockdown combined with miR-373 overexpression yielded optimal tumor suppressive effects and the lowest VM density in vivo.
HOXA-AS2 knockdown inhibited malignant glioma behaviors and VM formation via the miR-373/EGFR axis. |
| doi_str_mv | 10.1159/000486253 |
| format | Article |
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Quantitative real-time PCR was performed to determine the expression levels of HOXA-AS2 in glioma samples and glioblastoma cell lines. CD34-periodic acid-Schiff dual-staining was performed to assess VM in glioma samples. CCK-8, transwell, and Matrigel tube formation assays were performed to measure the effects of HOXA-AS2 knockdown on cell viability, migration, invasion, and VM tube formation, respectively. RNA immunoprecipitation, dual-luciferase reporter and Western blot assays were performed to explore the molecular mechanisms underlying the functions of HOXS-AS2 in glioblastoma cells. A nude mouse xenograft model was used to investigate the role of HOXA-AS2 in xenograft glioma growth and VM density. Student's t-tests, one-way ANOVAs followed by Bonferroni posthoc tests, and chi-square tests were used for the statistical analyses.
HOXA-AS2 was upregulated in glioma samples and cell lines and was positively correlated with VM. HOXA-AS2 knockdown attenuated cell viability, migration, invasion, and VM formation in glioma cells and inhibited the expression of vascular endothelial-cadherin (VE-cadherin), as well as the expression and activity of matrix metalloproteinase matrix metalloproteinase (MMP)-2 and MMP-9. miR-373 was downregulated in glioma samples and cell lines and suppressed malignancy in glioblastoma cells. HOXA-AS2 bound to miR-373 and negatively regulated its expression. Epidermal growth factor receptor (EGFR), a target of miR-373, increased the expression levels of VE-cadherin, as well as the expression and activity levels of MMP-2 and MMP-9, via activating phosphatidylinositol 3-kinase/serine/threonine kinase pathways. HOXA-AS2 knockdown combined with miR-373 overexpression yielded optimal tumor suppressive effects and the lowest VM density in vivo.
HOXA-AS2 knockdown inhibited malignant glioma behaviors and VM formation via the miR-373/EGFR axis.</description><identifier>ISSN: 1015-8987</identifier><identifier>EISSN: 1421-9778</identifier><identifier>DOI: 10.1159/000486253</identifier><identifier>PMID: 29310118</identifier><language>eng</language><publisher>Basel, Switzerland: S. Karger AG</publisher><subject>Animals ; Biotechnology ; Brain - metabolism ; Brain - pathology ; Brain Neoplasms - blood supply ; Brain Neoplasms - metabolism ; Brain Neoplasms - pathology ; Breast cancer ; Cell adhesion & migration ; Cell growth ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; EGFR ; Epidermal growth factor ; ErbB Receptors - antagonists & inhibitors ; ErbB Receptors - genetics ; ErbB Receptors - metabolism ; Gene expression ; Glioma ; Glioma - blood supply ; Glioma - metabolism ; Glioma - pathology ; HOXA-AS2 ; Humans ; Kinases ; Long non-coding RNA ; Male ; Matrix Metalloproteinase 2 - metabolism ; Matrix Metalloproteinase 9 - metabolism ; Metastasis ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; MicroRNA ; MicroRNAs ; MicroRNAs - genetics ; MicroRNAs - metabolism ; MiR-373 ; Neovascularization, Pathologic ; Phosphatidylinositol 3-Kinases - metabolism ; Prostate cancer ; Retracted Paper ; RNA Interference ; RNA, Long Noncoding - antagonists & inhibitors ; RNA, Long Noncoding - genetics ; RNA, Long Noncoding - metabolism ; Up-Regulation ; Vasculogenic mimicry</subject><ispartof>Cellular physiology and biochemistry, 2018-01, Vol.45 (1), p.131-147</ispartof><rights>2018 The Author(s). Published by S. Karger AG, Basel</rights><rights>2018 The Author(s). Published by S. Karger AG, Basel.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c463t-b3387865116cd6870b8f89906c2d48187c3d486f164e858c882a889bc90583713</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,864,2102,27635,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29310118$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gao, Yana</creatorcontrib><creatorcontrib>Yu, Hai</creatorcontrib><creatorcontrib>Liu, Yunhui</creatorcontrib><creatorcontrib>Liu, Xiaobai</creatorcontrib><creatorcontrib>Zheng, Jian</creatorcontrib><creatorcontrib>Ma, Jun</creatorcontrib><creatorcontrib>Gong, Wei</creatorcontrib><creatorcontrib>Chen, Jiajia</creatorcontrib><creatorcontrib>Zhao, Lini</creatorcontrib><creatorcontrib>Tian, Yu</creatorcontrib><creatorcontrib>Xue, Yixue</creatorcontrib><title>Long Non-Coding RNA HOXA-AS2 Regulates Malignant Glioma Behaviors and Vasculogenic Mimicry Formation via the MiR-373/EGFR Axis</title><title>Cellular physiology and biochemistry</title><addtitle>Cell Physiol Biochem</addtitle><description>Vasculogenic mimicry (VM) has been reported to be a novel glioma neovascularization process. Anti-VM therapy provides new insight into glioma clinical management. In this study, we revealed the role of the long non-coding RNA HOXA cluster antisense RNA 2 (HOXA-AS2) in malignant glioma behaviors and VM formation.
Quantitative real-time PCR was performed to determine the expression levels of HOXA-AS2 in glioma samples and glioblastoma cell lines. CD34-periodic acid-Schiff dual-staining was performed to assess VM in glioma samples. CCK-8, transwell, and Matrigel tube formation assays were performed to measure the effects of HOXA-AS2 knockdown on cell viability, migration, invasion, and VM tube formation, respectively. RNA immunoprecipitation, dual-luciferase reporter and Western blot assays were performed to explore the molecular mechanisms underlying the functions of HOXS-AS2 in glioblastoma cells. A nude mouse xenograft model was used to investigate the role of HOXA-AS2 in xenograft glioma growth and VM density. Student's t-tests, one-way ANOVAs followed by Bonferroni posthoc tests, and chi-square tests were used for the statistical analyses.
HOXA-AS2 was upregulated in glioma samples and cell lines and was positively correlated with VM. HOXA-AS2 knockdown attenuated cell viability, migration, invasion, and VM formation in glioma cells and inhibited the expression of vascular endothelial-cadherin (VE-cadherin), as well as the expression and activity of matrix metalloproteinase matrix metalloproteinase (MMP)-2 and MMP-9. miR-373 was downregulated in glioma samples and cell lines and suppressed malignancy in glioblastoma cells. HOXA-AS2 bound to miR-373 and negatively regulated its expression. Epidermal growth factor receptor (EGFR), a target of miR-373, increased the expression levels of VE-cadherin, as well as the expression and activity levels of MMP-2 and MMP-9, via activating phosphatidylinositol 3-kinase/serine/threonine kinase pathways. HOXA-AS2 knockdown combined with miR-373 overexpression yielded optimal tumor suppressive effects and the lowest VM density in vivo.
HOXA-AS2 knockdown inhibited malignant glioma behaviors and VM formation via the miR-373/EGFR axis.</description><subject>Animals</subject><subject>Biotechnology</subject><subject>Brain - metabolism</subject><subject>Brain - pathology</subject><subject>Brain Neoplasms - blood supply</subject><subject>Brain Neoplasms - metabolism</subject><subject>Brain Neoplasms - pathology</subject><subject>Breast cancer</subject><subject>Cell adhesion & migration</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement</subject><subject>Cell Proliferation</subject><subject>EGFR</subject><subject>Epidermal growth factor</subject><subject>ErbB Receptors - antagonists & inhibitors</subject><subject>ErbB Receptors - genetics</subject><subject>ErbB Receptors - metabolism</subject><subject>Gene expression</subject><subject>Glioma</subject><subject>Glioma - blood supply</subject><subject>Glioma - metabolism</subject><subject>Glioma - pathology</subject><subject>HOXA-AS2</subject><subject>Humans</subject><subject>Kinases</subject><subject>Long non-coding RNA</subject><subject>Male</subject><subject>Matrix Metalloproteinase 2 - metabolism</subject><subject>Matrix Metalloproteinase 9 - metabolism</subject><subject>Metastasis</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Nude</subject><subject>MicroRNA</subject><subject>MicroRNAs</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>MiR-373</subject><subject>Neovascularization, Pathologic</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Prostate cancer</subject><subject>Retracted Paper</subject><subject>RNA Interference</subject><subject>RNA, Long Noncoding - antagonists & inhibitors</subject><subject>RNA, Long Noncoding - genetics</subject><subject>RNA, Long Noncoding - metabolism</subject><subject>Up-Regulation</subject><subject>Vasculogenic mimicry</subject><issn>1015-8987</issn><issn>1421-9778</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>M--</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DOA</sourceid><recordid>eNptkc9v0zAUxyMEYmNw4I6QJS5wCLPj2H4-dtXaTeo2VH6Im-U4TuaSxMVOJnbhb8ejpUiI03v2--jzbH2z7CXB7wlh8hRjXAIvGH2UHZOyILkUAh6nHhOWgwRxlD2LcYPTUcjiaXZUSJpmBI6znys_tOjaD_nc1y616-sZurj5OstnHwu0tu3U6dFGdKU71w56GNGyc77X6Mze6jvnQ0R6qNEXHc3U-dYOzqAr1zsT7tHCh16Pzg_ozmk03to0WedU0NPz5WKNZj9cfJ49aXQX7Yt9Pck-L84_zS_y1c3ycj5b5abkdMwrSkEAZ4RwU3MQuIIGpMTcFHUJBIShqfKG8NICAwNQaABZGYkZUEHoSXa589Zeb9Q2uF6He-W1U78vfGiVDqMznVUaONVVbUtGcElsAZW01BJCRcOBSZxcb3eubfDfJxtH1btobNfpwfopKiJBMlbKskzom3_QjZ_CkH6qCkIE4aygD8J3O8oEH2OwzeGBBKuHgNUh4MS-3hunqrf1gfyT6N-V33RobTgA8w9nO4Xa1k2iXv2X2m_5BXgOr2M</recordid><startdate>20180101</startdate><enddate>20180101</enddate><creator>Gao, Yana</creator><creator>Yu, Hai</creator><creator>Liu, Yunhui</creator><creator>Liu, Xiaobai</creator><creator>Zheng, Jian</creator><creator>Ma, Jun</creator><creator>Gong, Wei</creator><creator>Chen, Jiajia</creator><creator>Zhao, Lini</creator><creator>Tian, Yu</creator><creator>Xue, Yixue</creator><general>S. Karger AG</general><general>Cell Physiol Biochem Press GmbH & Co KG</general><scope>M--</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>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>DOA</scope></search><sort><creationdate>20180101</creationdate><title>Long Non-Coding RNA HOXA-AS2 Regulates Malignant Glioma Behaviors and Vasculogenic Mimicry Formation via the MiR-373/EGFR Axis</title><author>Gao, Yana ; Yu, Hai ; Liu, Yunhui ; Liu, Xiaobai ; Zheng, Jian ; Ma, Jun ; Gong, Wei ; Chen, Jiajia ; Zhao, Lini ; Tian, Yu ; Xue, Yixue</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c463t-b3387865116cd6870b8f89906c2d48187c3d486f164e858c882a889bc90583713</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Animals</topic><topic>Biotechnology</topic><topic>Brain - metabolism</topic><topic>Brain - pathology</topic><topic>Brain Neoplasms - blood supply</topic><topic>Brain Neoplasms - metabolism</topic><topic>Brain Neoplasms - pathology</topic><topic>Breast cancer</topic><topic>Cell adhesion & migration</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement</topic><topic>Cell Proliferation</topic><topic>EGFR</topic><topic>Epidermal growth factor</topic><topic>ErbB Receptors - antagonists & inhibitors</topic><topic>ErbB Receptors - genetics</topic><topic>ErbB Receptors - metabolism</topic><topic>Gene expression</topic><topic>Glioma</topic><topic>Glioma - blood supply</topic><topic>Glioma - metabolism</topic><topic>Glioma - pathology</topic><topic>HOXA-AS2</topic><topic>Humans</topic><topic>Kinases</topic><topic>Long non-coding RNA</topic><topic>Male</topic><topic>Matrix Metalloproteinase 2 - metabolism</topic><topic>Matrix Metalloproteinase 9 - metabolism</topic><topic>Metastasis</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Nude</topic><topic>MicroRNA</topic><topic>MicroRNAs</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>MiR-373</topic><topic>Neovascularization, Pathologic</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>Prostate cancer</topic><topic>Retracted Paper</topic><topic>RNA Interference</topic><topic>RNA, Long Noncoding - antagonists & inhibitors</topic><topic>RNA, Long Noncoding - genetics</topic><topic>RNA, Long Noncoding - metabolism</topic><topic>Up-Regulation</topic><topic>Vasculogenic mimicry</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gao, Yana</creatorcontrib><creatorcontrib>Yu, Hai</creatorcontrib><creatorcontrib>Liu, Yunhui</creatorcontrib><creatorcontrib>Liu, Xiaobai</creatorcontrib><creatorcontrib>Zheng, Jian</creatorcontrib><creatorcontrib>Ma, Jun</creatorcontrib><creatorcontrib>Gong, Wei</creatorcontrib><creatorcontrib>Chen, Jiajia</creatorcontrib><creatorcontrib>Zhao, Lini</creatorcontrib><creatorcontrib>Tian, Yu</creatorcontrib><creatorcontrib>Xue, Yixue</creatorcontrib><collection>Karger Open Access Journals</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>Health & Medical Collection</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 Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</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>Medical 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>DOAJ Directory of Open Access Journals</collection><jtitle>Cellular physiology and biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gao, Yana</au><au>Yu, Hai</au><au>Liu, Yunhui</au><au>Liu, Xiaobai</au><au>Zheng, Jian</au><au>Ma, Jun</au><au>Gong, Wei</au><au>Chen, Jiajia</au><au>Zhao, Lini</au><au>Tian, Yu</au><au>Xue, Yixue</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Long Non-Coding RNA HOXA-AS2 Regulates Malignant Glioma Behaviors and Vasculogenic Mimicry Formation via the MiR-373/EGFR Axis</atitle><jtitle>Cellular physiology and biochemistry</jtitle><addtitle>Cell Physiol Biochem</addtitle><date>2018-01-01</date><risdate>2018</risdate><volume>45</volume><issue>1</issue><spage>131</spage><epage>147</epage><pages>131-147</pages><issn>1015-8987</issn><eissn>1421-9778</eissn><abstract>Vasculogenic mimicry (VM) has been reported to be a novel glioma neovascularization process. Anti-VM therapy provides new insight into glioma clinical management. In this study, we revealed the role of the long non-coding RNA HOXA cluster antisense RNA 2 (HOXA-AS2) in malignant glioma behaviors and VM formation.
Quantitative real-time PCR was performed to determine the expression levels of HOXA-AS2 in glioma samples and glioblastoma cell lines. CD34-periodic acid-Schiff dual-staining was performed to assess VM in glioma samples. CCK-8, transwell, and Matrigel tube formation assays were performed to measure the effects of HOXA-AS2 knockdown on cell viability, migration, invasion, and VM tube formation, respectively. RNA immunoprecipitation, dual-luciferase reporter and Western blot assays were performed to explore the molecular mechanisms underlying the functions of HOXS-AS2 in glioblastoma cells. A nude mouse xenograft model was used to investigate the role of HOXA-AS2 in xenograft glioma growth and VM density. Student's t-tests, one-way ANOVAs followed by Bonferroni posthoc tests, and chi-square tests were used for the statistical analyses.
HOXA-AS2 was upregulated in glioma samples and cell lines and was positively correlated with VM. HOXA-AS2 knockdown attenuated cell viability, migration, invasion, and VM formation in glioma cells and inhibited the expression of vascular endothelial-cadherin (VE-cadherin), as well as the expression and activity of matrix metalloproteinase matrix metalloproteinase (MMP)-2 and MMP-9. miR-373 was downregulated in glioma samples and cell lines and suppressed malignancy in glioblastoma cells. HOXA-AS2 bound to miR-373 and negatively regulated its expression. Epidermal growth factor receptor (EGFR), a target of miR-373, increased the expression levels of VE-cadherin, as well as the expression and activity levels of MMP-2 and MMP-9, via activating phosphatidylinositol 3-kinase/serine/threonine kinase pathways. HOXA-AS2 knockdown combined with miR-373 overexpression yielded optimal tumor suppressive effects and the lowest VM density in vivo.
HOXA-AS2 knockdown inhibited malignant glioma behaviors and VM formation via the miR-373/EGFR axis.</abstract><cop>Basel, Switzerland</cop><pub>S. Karger AG</pub><pmid>29310118</pmid><doi>10.1159/000486253</doi><tpages>17</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Biotechnology Brain - metabolism Brain - pathology Brain Neoplasms - blood supply Brain Neoplasms - metabolism Brain Neoplasms - pathology Breast cancer Cell adhesion & migration Cell growth Cell Line, Tumor Cell Movement Cell Proliferation EGFR Epidermal growth factor ErbB Receptors - antagonists & inhibitors ErbB Receptors - genetics ErbB Receptors - metabolism Gene expression Glioma Glioma - blood supply Glioma - metabolism Glioma - pathology HOXA-AS2 Humans Kinases Long non-coding RNA Male Matrix Metalloproteinase 2 - metabolism Matrix Metalloproteinase 9 - metabolism Metastasis Mice Mice, Inbred BALB C Mice, Nude MicroRNA MicroRNAs MicroRNAs - genetics MicroRNAs - metabolism MiR-373 Neovascularization, Pathologic Phosphatidylinositol 3-Kinases - metabolism Prostate cancer Retracted Paper RNA Interference RNA, Long Noncoding - antagonists & inhibitors RNA, Long Noncoding - genetics RNA, Long Noncoding - metabolism Up-Regulation Vasculogenic mimicry |
| title | Long Non-Coding RNA HOXA-AS2 Regulates Malignant Glioma Behaviors and Vasculogenic Mimicry Formation via the MiR-373/EGFR Axis |
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