OSCC Exosomes Regulate miR-210-3p Targeting EFNA3 to Promote Oral Cancer Angiogenesis through the PI3K/AKT Pathway
This study is aimed at determining how oral squamous cell carcinoma (OSCC) regulates the angiogenesis of HUVECs through miR-210-3p expression and exploring the relationship among miR-210-3p, its target protein, and the possible mechanism of angiogenesis regulation. miR-210-3p expression was detected...
Gespeichert in:
| Veröffentlicht in: | BioMed research international 2020, Vol.2020 (2020), p.1-13 |
|---|---|
| Hauptverfasser: | , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 13 |
|---|---|
| container_issue | 2020 |
| container_start_page | 1 |
| container_title | BioMed research international |
| container_volume | 2020 |
| creator | Shang, Zhengjun Shao, Zhe Jiang, Erhui Liu, Ke Luo, Xinyue Zhou, Xiao-cheng Wang, Lin Wang, Hui Chen, Yang |
| description | This study is aimed at determining how oral squamous cell carcinoma (OSCC) regulates the angiogenesis of HUVECs through miR-210-3p expression and exploring the relationship among miR-210-3p, its target protein, and the possible mechanism of angiogenesis regulation. miR-210-3p expression was detected in OSCC tissues and juxta cancerous tissues (JCT), and the relationship among miR-210-3p, microvessel density (MVD), and histopathologic features was analyzed. A conditioned medium (CM) of the OSCC cell line CAL27 was collected to stimulate human umbilical vein endothelial cells (HUVECs), and the miR-210-3p levels and tube formation capability of HUVECs were measured. The target protein level of miR-210-3p was altered; then, PI3K/AKT pathway activation in HUVECs was detected. miR-210-3p was tested in exosomes separated from CAL27 CM, and the transfer of miR-210-3p from OSCC exosomes to HUVECs was verified. Then, we found that the OSCC tissues had higher miR-210-3p levels than the JCT, and miR-210-3p level was positively correlated with MVD and tumor grade. CAL27 CM was able to elevate miR-210-3p levels in HUVECs and promoted tube formation. EFNA3 was the target gene of miR-210-3p, and ephrinA3 protein level was able to influence the migration and proliferation of HUVECs. The levels of phosphorylated AKT in the HUVECs increased when ephrinA3 was downregulated, and the upregulation of ephrinA3 resulted in the suppression of the PI3K/AKT pathway. miR-210-3p was detected in exosomes isolated from the CM of CAL27 cells, and miR-210-3p level in the HUVECs was elevated after absorbing the OSCC exosomes. In conclusion, miR-210-3p was more overexpressed in OSCC tissues than in the JCT. The exosomes secreted by OSCC cells were able to upregulate miR-210-3p expression and reduce ephrinA3 expression in HUVECs and promoted tube formation through the PI3K/AKT signaling pathway. |
| doi_str_mv | 10.1155/2020/2125656 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_7368228</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A639879968</galeid><sourcerecordid>A639879968</sourcerecordid><originalsourceid>FETCH-LOGICAL-c499t-9cfb0bab54796912453f5bcf5599d27e18ff3f0655a8747b56cc700ff6d0e0033</originalsourceid><addsrcrecordid>eNqNkc9r2zAYhs3YaEvXW89DsOPqRj8sWboMjEnX0rKELjsLWZFsldjKJHtd__spJEu3277L98H38PDCm2WXCF4jROkMQwxnGGHKKHuTnWGCipyhAr093oScZhcxPsE0HDEo2El2SjATlCN4loXFt7oG818--t5E8GjaaaNGA3r3mGMEc7IFKxVaM7qhBfObrxUBowfL4HufqEVQG1CrQZsAqqF1vjWDiS6CsQt-aru0DVjekftZdb8CSzV2z-rlffbOqk00F4d9nn2_ma_q2_xh8eWurh5yXQgx5kLbBjaqoUUpmEC4oMTSRltKhVjj0iBuLbGQUap4WZQNZVqXEFrL1tBASMh59nnv3U5Nb9baDGOKK7fB9Sq8SK-c_PczuE62_qcsCeMY8yT4eBAE_2MycZRPfgpDyixxgQtecsbhK9WqjZFusD7JdO-ilhUjgpdCsJ3rak_p4GMMxh5zICh3VcpdlfJQZcI__J39CP8pLgGf9kDnhrV6dv-pM4kxVr3SiGCS5jd9Pay0</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2424878680</pqid></control><display><type>article</type><title>OSCC Exosomes Regulate miR-210-3p Targeting EFNA3 to Promote Oral Cancer Angiogenesis through the PI3K/AKT Pathway</title><source>MEDLINE</source><source>PubMed Central Open Access</source><source>Wiley-Blackwell Open Access Titles</source><source>PubMed Central</source><source>Alma/SFX Local Collection</source><creator>Shang, Zhengjun ; Shao, Zhe ; Jiang, Erhui ; Liu, Ke ; Luo, Xinyue ; Zhou, Xiao-cheng ; Wang, Lin ; Wang, Hui ; Chen, Yang</creator><contributor>Hamburger, Anne ; Anne Hamburger</contributor><creatorcontrib>Shang, Zhengjun ; Shao, Zhe ; Jiang, Erhui ; Liu, Ke ; Luo, Xinyue ; Zhou, Xiao-cheng ; Wang, Lin ; Wang, Hui ; Chen, Yang ; Hamburger, Anne ; Anne Hamburger</creatorcontrib><description>This study is aimed at determining how oral squamous cell carcinoma (OSCC) regulates the angiogenesis of HUVECs through miR-210-3p expression and exploring the relationship among miR-210-3p, its target protein, and the possible mechanism of angiogenesis regulation. miR-210-3p expression was detected in OSCC tissues and juxta cancerous tissues (JCT), and the relationship among miR-210-3p, microvessel density (MVD), and histopathologic features was analyzed. A conditioned medium (CM) of the OSCC cell line CAL27 was collected to stimulate human umbilical vein endothelial cells (HUVECs), and the miR-210-3p levels and tube formation capability of HUVECs were measured. The target protein level of miR-210-3p was altered; then, PI3K/AKT pathway activation in HUVECs was detected. miR-210-3p was tested in exosomes separated from CAL27 CM, and the transfer of miR-210-3p from OSCC exosomes to HUVECs was verified. Then, we found that the OSCC tissues had higher miR-210-3p levels than the JCT, and miR-210-3p level was positively correlated with MVD and tumor grade. CAL27 CM was able to elevate miR-210-3p levels in HUVECs and promoted tube formation. EFNA3 was the target gene of miR-210-3p, and ephrinA3 protein level was able to influence the migration and proliferation of HUVECs. The levels of phosphorylated AKT in the HUVECs increased when ephrinA3 was downregulated, and the upregulation of ephrinA3 resulted in the suppression of the PI3K/AKT pathway. miR-210-3p was detected in exosomes isolated from the CM of CAL27 cells, and miR-210-3p level in the HUVECs was elevated after absorbing the OSCC exosomes. In conclusion, miR-210-3p was more overexpressed in OSCC tissues than in the JCT. The exosomes secreted by OSCC cells were able to upregulate miR-210-3p expression and reduce ephrinA3 expression in HUVECs and promoted tube formation through the PI3K/AKT signaling pathway.</description><identifier>ISSN: 2314-6133</identifier><identifier>EISSN: 2314-6141</identifier><identifier>DOI: 10.1155/2020/2125656</identifier><identifier>PMID: 32695810</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>1-Phosphatidylinositol 3-kinase ; AKT protein ; Angiogenesis ; Antibodies ; Base Sequence ; Cancer ; Cancer therapies ; Carcinoma, Squamous Cell - genetics ; Carcinoma, Squamous Cell - pathology ; Cell growth ; Cell Line, Tumor ; Cell Movement - drug effects ; Cell Proliferation - drug effects ; Chromosome 3 ; Culture Media, Conditioned - pharmacology ; Cybernetics ; Dehydrogenases ; Endothelial cells ; Ephrin-A3 - genetics ; Ephrin-A3 - metabolism ; Exosomes ; Exosomes - metabolism ; Gene expression ; Gene Expression Regulation, Neoplastic - drug effects ; Genetic aspects ; Health aspects ; Human Umbilical Vein Endothelial Cells - drug effects ; Human Umbilical Vein Endothelial Cells - metabolism ; Humans ; Level (quantity) ; MicroRNA ; MicroRNAs ; MicroRNAs - genetics ; MicroRNAs - metabolism ; Microvessels - pathology ; Mouth cancer ; Mouth Neoplasms - genetics ; Mouth Neoplasms - pathology ; Neovascularization ; Neovascularization, Pathologic - genetics ; Oral cancer ; Oral squamous cell carcinoma ; Phosphatidylinositol 3-Kinases - metabolism ; Proteins ; Proto-Oncogene Proteins c-akt - metabolism ; Signal Transduction ; Squamous cell carcinoma ; Tissues ; Tumors ; Umbilical vein ; Up-Regulation - drug effects</subject><ispartof>BioMed research international, 2020, Vol.2020 (2020), p.1-13</ispartof><rights>Copyright © 2020 Hui Wang et al.</rights><rights>COPYRIGHT 2020 John Wiley & Sons, Inc.</rights><rights>Copyright © 2020 Hui Wang 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. http://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2020 Hui Wang et al. 2020</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c499t-9cfb0bab54796912453f5bcf5599d27e18ff3f0655a8747b56cc700ff6d0e0033</citedby><cites>FETCH-LOGICAL-c499t-9cfb0bab54796912453f5bcf5599d27e18ff3f0655a8747b56cc700ff6d0e0033</cites><orcidid>0000-0003-4668-026X ; 0000-0002-4884-8129 ; 0000-0003-2357-3760</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/PMC7368228/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7368228/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,4024,27923,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32695810$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Hamburger, Anne</contributor><contributor>Anne Hamburger</contributor><creatorcontrib>Shang, Zhengjun</creatorcontrib><creatorcontrib>Shao, Zhe</creatorcontrib><creatorcontrib>Jiang, Erhui</creatorcontrib><creatorcontrib>Liu, Ke</creatorcontrib><creatorcontrib>Luo, Xinyue</creatorcontrib><creatorcontrib>Zhou, Xiao-cheng</creatorcontrib><creatorcontrib>Wang, Lin</creatorcontrib><creatorcontrib>Wang, Hui</creatorcontrib><creatorcontrib>Chen, Yang</creatorcontrib><title>OSCC Exosomes Regulate miR-210-3p Targeting EFNA3 to Promote Oral Cancer Angiogenesis through the PI3K/AKT Pathway</title><title>BioMed research international</title><addtitle>Biomed Res Int</addtitle><description>This study is aimed at determining how oral squamous cell carcinoma (OSCC) regulates the angiogenesis of HUVECs through miR-210-3p expression and exploring the relationship among miR-210-3p, its target protein, and the possible mechanism of angiogenesis regulation. miR-210-3p expression was detected in OSCC tissues and juxta cancerous tissues (JCT), and the relationship among miR-210-3p, microvessel density (MVD), and histopathologic features was analyzed. A conditioned medium (CM) of the OSCC cell line CAL27 was collected to stimulate human umbilical vein endothelial cells (HUVECs), and the miR-210-3p levels and tube formation capability of HUVECs were measured. The target protein level of miR-210-3p was altered; then, PI3K/AKT pathway activation in HUVECs was detected. miR-210-3p was tested in exosomes separated from CAL27 CM, and the transfer of miR-210-3p from OSCC exosomes to HUVECs was verified. Then, we found that the OSCC tissues had higher miR-210-3p levels than the JCT, and miR-210-3p level was positively correlated with MVD and tumor grade. CAL27 CM was able to elevate miR-210-3p levels in HUVECs and promoted tube formation. EFNA3 was the target gene of miR-210-3p, and ephrinA3 protein level was able to influence the migration and proliferation of HUVECs. The levels of phosphorylated AKT in the HUVECs increased when ephrinA3 was downregulated, and the upregulation of ephrinA3 resulted in the suppression of the PI3K/AKT pathway. miR-210-3p was detected in exosomes isolated from the CM of CAL27 cells, and miR-210-3p level in the HUVECs was elevated after absorbing the OSCC exosomes. In conclusion, miR-210-3p was more overexpressed in OSCC tissues than in the JCT. The exosomes secreted by OSCC cells were able to upregulate miR-210-3p expression and reduce ephrinA3 expression in HUVECs and promoted tube formation through the PI3K/AKT signaling pathway.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>AKT protein</subject><subject>Angiogenesis</subject><subject>Antibodies</subject><subject>Base Sequence</subject><subject>Cancer</subject><subject>Cancer therapies</subject><subject>Carcinoma, Squamous Cell - genetics</subject><subject>Carcinoma, Squamous Cell - pathology</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement - drug effects</subject><subject>Cell Proliferation - drug effects</subject><subject>Chromosome 3</subject><subject>Culture Media, Conditioned - pharmacology</subject><subject>Cybernetics</subject><subject>Dehydrogenases</subject><subject>Endothelial cells</subject><subject>Ephrin-A3 - genetics</subject><subject>Ephrin-A3 - metabolism</subject><subject>Exosomes</subject><subject>Exosomes - metabolism</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic - drug effects</subject><subject>Genetic aspects</subject><subject>Health aspects</subject><subject>Human Umbilical Vein Endothelial Cells - drug effects</subject><subject>Human Umbilical Vein Endothelial Cells - metabolism</subject><subject>Humans</subject><subject>Level (quantity)</subject><subject>MicroRNA</subject><subject>MicroRNAs</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>Microvessels - pathology</subject><subject>Mouth cancer</subject><subject>Mouth Neoplasms - genetics</subject><subject>Mouth Neoplasms - pathology</subject><subject>Neovascularization</subject><subject>Neovascularization, Pathologic - genetics</subject><subject>Oral cancer</subject><subject>Oral squamous cell carcinoma</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Signal Transduction</subject><subject>Squamous cell carcinoma</subject><subject>Tissues</subject><subject>Tumors</subject><subject>Umbilical vein</subject><subject>Up-Regulation - drug effects</subject><issn>2314-6133</issn><issn>2314-6141</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>RHX</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>eNqNkc9r2zAYhs3YaEvXW89DsOPqRj8sWboMjEnX0rKELjsLWZFsldjKJHtd__spJEu3277L98H38PDCm2WXCF4jROkMQwxnGGHKKHuTnWGCipyhAr093oScZhcxPsE0HDEo2El2SjATlCN4loXFt7oG818--t5E8GjaaaNGA3r3mGMEc7IFKxVaM7qhBfObrxUBowfL4HufqEVQG1CrQZsAqqF1vjWDiS6CsQt-aru0DVjekftZdb8CSzV2z-rlffbOqk00F4d9nn2_ma_q2_xh8eWurh5yXQgx5kLbBjaqoUUpmEC4oMTSRltKhVjj0iBuLbGQUap4WZQNZVqXEFrL1tBASMh59nnv3U5Nb9baDGOKK7fB9Sq8SK-c_PczuE62_qcsCeMY8yT4eBAE_2MycZRPfgpDyixxgQtecsbhK9WqjZFusD7JdO-ilhUjgpdCsJ3rak_p4GMMxh5zICh3VcpdlfJQZcI__J39CP8pLgGf9kDnhrV6dv-pM4kxVr3SiGCS5jd9Pay0</recordid><startdate>2020</startdate><enddate>2020</enddate><creator>Shang, Zhengjun</creator><creator>Shao, Zhe</creator><creator>Jiang, Erhui</creator><creator>Liu, Ke</creator><creator>Luo, Xinyue</creator><creator>Zhou, Xiao-cheng</creator><creator>Wang, Lin</creator><creator>Wang, Hui</creator><creator>Chen, Yang</creator><general>Hindawi Publishing Corporation</general><general>Hindawi</general><general>John Wiley & Sons, Inc</general><general>Hindawi Limited</general><scope>ADJCN</scope><scope>AHFXO</scope><scope>RHU</scope><scope>RHW</scope><scope>RHX</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>7QL</scope><scope>7QO</scope><scope>7T7</scope><scope>7TK</scope><scope>7U7</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>CWDGH</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-4668-026X</orcidid><orcidid>https://orcid.org/0000-0002-4884-8129</orcidid><orcidid>https://orcid.org/0000-0003-2357-3760</orcidid></search><sort><creationdate>2020</creationdate><title>OSCC Exosomes Regulate miR-210-3p Targeting EFNA3 to Promote Oral Cancer Angiogenesis through the PI3K/AKT Pathway</title><author>Shang, Zhengjun ; Shao, Zhe ; Jiang, Erhui ; Liu, Ke ; Luo, Xinyue ; Zhou, Xiao-cheng ; Wang, Lin ; Wang, Hui ; Chen, Yang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c499t-9cfb0bab54796912453f5bcf5599d27e18ff3f0655a8747b56cc700ff6d0e0033</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>AKT protein</topic><topic>Angiogenesis</topic><topic>Antibodies</topic><topic>Base Sequence</topic><topic>Cancer</topic><topic>Cancer therapies</topic><topic>Carcinoma, Squamous Cell - genetics</topic><topic>Carcinoma, Squamous Cell - pathology</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement - drug effects</topic><topic>Cell Proliferation - drug effects</topic><topic>Chromosome 3</topic><topic>Culture Media, Conditioned - pharmacology</topic><topic>Cybernetics</topic><topic>Dehydrogenases</topic><topic>Endothelial cells</topic><topic>Ephrin-A3 - genetics</topic><topic>Ephrin-A3 - metabolism</topic><topic>Exosomes</topic><topic>Exosomes - metabolism</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Neoplastic - drug effects</topic><topic>Genetic aspects</topic><topic>Health aspects</topic><topic>Human Umbilical Vein Endothelial Cells - drug effects</topic><topic>Human Umbilical Vein Endothelial Cells - metabolism</topic><topic>Humans</topic><topic>Level (quantity)</topic><topic>MicroRNA</topic><topic>MicroRNAs</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>Microvessels - pathology</topic><topic>Mouth cancer</topic><topic>Mouth Neoplasms - genetics</topic><topic>Mouth Neoplasms - pathology</topic><topic>Neovascularization</topic><topic>Neovascularization, Pathologic - genetics</topic><topic>Oral cancer</topic><topic>Oral squamous cell carcinoma</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>Proteins</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Signal Transduction</topic><topic>Squamous cell carcinoma</topic><topic>Tissues</topic><topic>Tumors</topic><topic>Umbilical vein</topic><topic>Up-Regulation - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shang, Zhengjun</creatorcontrib><creatorcontrib>Shao, Zhe</creatorcontrib><creatorcontrib>Jiang, Erhui</creatorcontrib><creatorcontrib>Liu, Ke</creatorcontrib><creatorcontrib>Luo, Xinyue</creatorcontrib><creatorcontrib>Zhou, Xiao-cheng</creatorcontrib><creatorcontrib>Wang, Lin</creatorcontrib><creatorcontrib>Wang, Hui</creatorcontrib><creatorcontrib>Chen, Yang</creatorcontrib><collection>الدوريات العلمية والإحصائية - e-Marefa Academic and Statistical Periodicals</collection><collection>معرفة - المحتوى العربي الأكاديمي المتكامل - e-Marefa Academic Complete</collection><collection>Hindawi Publishing Complete</collection><collection>Hindawi Publishing Subscription Journals</collection><collection>Hindawi Publishing 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>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology 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>Advanced Technologies & Aerospace Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>Middle East & Africa Database</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>AIDS and Cancer Research Abstracts</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>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</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>PubMed Central (Full Participant titles)</collection><jtitle>BioMed research international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Shang, Zhengjun</au><au>Shao, Zhe</au><au>Jiang, Erhui</au><au>Liu, Ke</au><au>Luo, Xinyue</au><au>Zhou, Xiao-cheng</au><au>Wang, Lin</au><au>Wang, Hui</au><au>Chen, Yang</au><au>Hamburger, Anne</au><au>Anne Hamburger</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>OSCC Exosomes Regulate miR-210-3p Targeting EFNA3 to Promote Oral Cancer Angiogenesis through the PI3K/AKT Pathway</atitle><jtitle>BioMed research international</jtitle><addtitle>Biomed Res Int</addtitle><date>2020</date><risdate>2020</risdate><volume>2020</volume><issue>2020</issue><spage>1</spage><epage>13</epage><pages>1-13</pages><issn>2314-6133</issn><eissn>2314-6141</eissn><abstract>This study is aimed at determining how oral squamous cell carcinoma (OSCC) regulates the angiogenesis of HUVECs through miR-210-3p expression and exploring the relationship among miR-210-3p, its target protein, and the possible mechanism of angiogenesis regulation. miR-210-3p expression was detected in OSCC tissues and juxta cancerous tissues (JCT), and the relationship among miR-210-3p, microvessel density (MVD), and histopathologic features was analyzed. A conditioned medium (CM) of the OSCC cell line CAL27 was collected to stimulate human umbilical vein endothelial cells (HUVECs), and the miR-210-3p levels and tube formation capability of HUVECs were measured. The target protein level of miR-210-3p was altered; then, PI3K/AKT pathway activation in HUVECs was detected. miR-210-3p was tested in exosomes separated from CAL27 CM, and the transfer of miR-210-3p from OSCC exosomes to HUVECs was verified. Then, we found that the OSCC tissues had higher miR-210-3p levels than the JCT, and miR-210-3p level was positively correlated with MVD and tumor grade. CAL27 CM was able to elevate miR-210-3p levels in HUVECs and promoted tube formation. EFNA3 was the target gene of miR-210-3p, and ephrinA3 protein level was able to influence the migration and proliferation of HUVECs. The levels of phosphorylated AKT in the HUVECs increased when ephrinA3 was downregulated, and the upregulation of ephrinA3 resulted in the suppression of the PI3K/AKT pathway. miR-210-3p was detected in exosomes isolated from the CM of CAL27 cells, and miR-210-3p level in the HUVECs was elevated after absorbing the OSCC exosomes. In conclusion, miR-210-3p was more overexpressed in OSCC tissues than in the JCT. The exosomes secreted by OSCC cells were able to upregulate miR-210-3p expression and reduce ephrinA3 expression in HUVECs and promoted tube formation through the PI3K/AKT signaling pathway.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>32695810</pmid><doi>10.1155/2020/2125656</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0003-4668-026X</orcidid><orcidid>https://orcid.org/0000-0002-4884-8129</orcidid><orcidid>https://orcid.org/0000-0003-2357-3760</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 2314-6133 |
| ispartof | BioMed research international, 2020, Vol.2020 (2020), p.1-13 |
| issn | 2314-6133 2314-6141 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_7368228 |
| source | MEDLINE; PubMed Central Open Access; Wiley-Blackwell Open Access Titles; PubMed Central; Alma/SFX Local Collection |
| subjects | 1-Phosphatidylinositol 3-kinase AKT protein Angiogenesis Antibodies Base Sequence Cancer Cancer therapies Carcinoma, Squamous Cell - genetics Carcinoma, Squamous Cell - pathology Cell growth Cell Line, Tumor Cell Movement - drug effects Cell Proliferation - drug effects Chromosome 3 Culture Media, Conditioned - pharmacology Cybernetics Dehydrogenases Endothelial cells Ephrin-A3 - genetics Ephrin-A3 - metabolism Exosomes Exosomes - metabolism Gene expression Gene Expression Regulation, Neoplastic - drug effects Genetic aspects Health aspects Human Umbilical Vein Endothelial Cells - drug effects Human Umbilical Vein Endothelial Cells - metabolism Humans Level (quantity) MicroRNA MicroRNAs MicroRNAs - genetics MicroRNAs - metabolism Microvessels - pathology Mouth cancer Mouth Neoplasms - genetics Mouth Neoplasms - pathology Neovascularization Neovascularization, Pathologic - genetics Oral cancer Oral squamous cell carcinoma Phosphatidylinositol 3-Kinases - metabolism Proteins Proto-Oncogene Proteins c-akt - metabolism Signal Transduction Squamous cell carcinoma Tissues Tumors Umbilical vein Up-Regulation - drug effects |
| title | OSCC Exosomes Regulate miR-210-3p Targeting EFNA3 to Promote Oral Cancer Angiogenesis through the PI3K/AKT Pathway |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-07T00%3A04%3A19IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=OSCC%20Exosomes%20Regulate%20miR-210-3p%20Targeting%20EFNA3%20to%20Promote%20Oral%20Cancer%20Angiogenesis%20through%20the%20PI3K/AKT%20Pathway&rft.jtitle=BioMed%20research%20international&rft.au=Shang,%20Zhengjun&rft.date=2020&rft.volume=2020&rft.issue=2020&rft.spage=1&rft.epage=13&rft.pages=1-13&rft.issn=2314-6133&rft.eissn=2314-6141&rft_id=info:doi/10.1155/2020/2125656&rft_dat=%3Cgale_pubme%3EA639879968%3C/gale_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2424878680&rft_id=info:pmid/32695810&rft_galeid=A639879968&rfr_iscdi=true |