Overexpression of MUC1 Enhances Proangiogenic Activity of Non-Small-Cell Lung Cancer Cells Through Activation of Akt and Extracellular Signal-regulated Kinase Pathways
Background Angiogenesis is an important process required for tumor progression. Mucin 1 (MUC1) is a transmembrane glycoprotein that is aberrantly upregulated in many types of cancer, including non-small-cell lung cancer (NSCLC). However, the biological significance of MUC1 overexpression in lung can...
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| Veröffentlicht in: | Lung 2011-12, Vol.189 (6), p.453-460 |
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| creator | Yao, Mengying Zhang, Weihong Zhang, Qingxian Xing, Lihua Xu, Aiguo Liu, Qiuhong Cui, Bing |
| description | Background
Angiogenesis is an important process required for tumor progression. Mucin 1 (MUC1) is a transmembrane glycoprotein that is aberrantly upregulated in many types of cancer, including non-small-cell lung cancer (NSCLC). However, the biological significance of MUC1 overexpression in lung cancer angiogenesis is not completely understood.
Methods
We showed that enforced expression of MUC1 in two NSCLC cell lines, A549 and NCI-H460, which have a low level of endogenous MUC1, promoted their ability to induce vascular endothelial growth factor (VEGF)-dependent endothelial cell migration and tube formation.
Results
There was a significant increase in VEGF expression in MUC1-overexpressing NSCLC cells. Moreover, MUC1 overexpression resulted in a marked elevation in phosphorylated Akt and extracellular signal-regulated kinase (ERK)1/2, indicative of activation of both signaling pathways. Most importantly, inhibition of Akt or ERK signaling using specific chemical inhibitors restrained the proangiogenic activity of MUC1-overexpressing NSCLC cells.
Conclusions
Taken together, our present data demonstrate that the aberrant upregulation of MUC1 favors tumor angiogenesis in NSCLC, likely through the activation of both Akt and ERK pathways and elevation of VEGF production. MUC1 may thus be a potential antiangiogenic target in NSCLC. |
| doi_str_mv | 10.1007/s00408-011-9327-y |
| format | Article |
| fullrecord | <record><control><sourceid>gale_proqu</sourceid><recordid>TN_cdi_proquest_miscellaneous_905681760</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A330803372</galeid><sourcerecordid>A330803372</sourcerecordid><originalsourceid>FETCH-LOGICAL-c572t-7122e303e4bb8925e31f65a4eae82228039b3238beba9959ec58542c5a41cd5f3</originalsourceid><addsrcrecordid>eNp1ks1u1DAUhSMEotPCA7BBFkiwcvFPPEmWo2goiIFWaru2nMxN4uKxp3ZSOk_Ea-KQ4adokBeWr79zdX18kuQFJaeUkOxdICQlOSaU4oKzDO8eJTOacoZpJsjjZEZ4SjGLzFFyHMINITSbU_E0OWK0EEUh0lny_fwOPNxvPYSgnUWuQZ-vS4qWtlO2hoAuvFO21a4Fq2u0qHt9p_vdyH1xFl9ulDG4BGPQarAtKkeRR2MhoKvOu6HtJpHq9-0XX3uk7Bot73uv6ggORnl0qVurDPbQxmMPa_RJWxUAXai--6Z24VnypFEmwPP9fpJcv19elR_w6vzsY7lY4VpkrMcZZQw44ZBWVV4wAZw2c6FSUJAzxnLCi4oznldQqWhAAbXIRcrqiNB6LRp-kryd-m69ux0g9HKjwzilsuCGIAsi5nm0kUTy1T_kjRt8fMRPiFAyn7MIvZ6gVhmQ2jZufPTYUi44J3Eeno0UPkBFx8Er4yw0OpYf8KcH-LjWsNH1QcGbvwQdKNN3wZlh_JPwEKQTWHsXgodGbr3eKL-TlMgxc3LKnIyZk2Pm5C5qXu6NGKoNrH8rfoUsAmwCQryyLfg_Tv2_6w-2rOBD</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>905010662</pqid></control><display><type>article</type><title>Overexpression of MUC1 Enhances Proangiogenic Activity of Non-Small-Cell Lung Cancer Cells Through Activation of Akt and Extracellular Signal-regulated Kinase Pathways</title><source>MEDLINE</source><source>SpringerNature Journals</source><creator>Yao, Mengying ; Zhang, Weihong ; Zhang, Qingxian ; Xing, Lihua ; Xu, Aiguo ; Liu, Qiuhong ; Cui, Bing</creator><creatorcontrib>Yao, Mengying ; Zhang, Weihong ; Zhang, Qingxian ; Xing, Lihua ; Xu, Aiguo ; Liu, Qiuhong ; Cui, Bing</creatorcontrib><description>Background
Angiogenesis is an important process required for tumor progression. Mucin 1 (MUC1) is a transmembrane glycoprotein that is aberrantly upregulated in many types of cancer, including non-small-cell lung cancer (NSCLC). However, the biological significance of MUC1 overexpression in lung cancer angiogenesis is not completely understood.
Methods
We showed that enforced expression of MUC1 in two NSCLC cell lines, A549 and NCI-H460, which have a low level of endogenous MUC1, promoted their ability to induce vascular endothelial growth factor (VEGF)-dependent endothelial cell migration and tube formation.
Results
There was a significant increase in VEGF expression in MUC1-overexpressing NSCLC cells. Moreover, MUC1 overexpression resulted in a marked elevation in phosphorylated Akt and extracellular signal-regulated kinase (ERK)1/2, indicative of activation of both signaling pathways. Most importantly, inhibition of Akt or ERK signaling using specific chemical inhibitors restrained the proangiogenic activity of MUC1-overexpressing NSCLC cells.
Conclusions
Taken together, our present data demonstrate that the aberrant upregulation of MUC1 favors tumor angiogenesis in NSCLC, likely through the activation of both Akt and ERK pathways and elevation of VEGF production. MUC1 may thus be a potential antiangiogenic target in NSCLC.</description><identifier>ISSN: 0341-2040</identifier><identifier>EISSN: 1432-1750</identifier><identifier>DOI: 10.1007/s00408-011-9327-y</identifier><identifier>PMID: 21959954</identifier><identifier>CODEN: LUNGD9</identifier><language>eng</language><publisher>New York: Springer-Verlag</publisher><subject>Angiogenesis ; Carcinoma, Non-Small-Cell Lung - blood supply ; Carcinoma, Non-Small-Cell Lung - metabolism ; Carcinoma, Non-Small-Cell Lung - pathology ; Cell Line, Tumor ; Cell Movement ; Chemical inhibitors ; Development and progression ; Endothelium, Vascular - metabolism ; Endothelium, Vascular - pathology ; Extracellular Signal-Regulated MAP Kinases - metabolism ; Gene Expression Regulation, Neoplastic ; Glycoproteins ; Humans ; Lung cancer ; Lung cancer, Non-small cell ; Lung Neoplasms - blood supply ; Lung Neoplasms - metabolism ; Lung Neoplasms - pathology ; MAP Kinase Signaling System - physiology ; Medicine ; Medicine & Public Health ; Mucin-1 - metabolism ; Mucins ; Neovascularization, Pathologic - metabolism ; Pneumology/Respiratory System ; Proto-Oncogene Proteins c-akt - metabolism ; Signal Transduction - physiology ; Up-Regulation ; Vascular endothelial growth factor ; Vascular Endothelial Growth Factor A - metabolism</subject><ispartof>Lung, 2011-12, Vol.189 (6), p.453-460</ispartof><rights>Springer Science+Business Media, LLC 2011</rights><rights>COPYRIGHT 2011 Springer</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c572t-7122e303e4bb8925e31f65a4eae82228039b3238beba9959ec58542c5a41cd5f3</citedby><cites>FETCH-LOGICAL-c572t-7122e303e4bb8925e31f65a4eae82228039b3238beba9959ec58542c5a41cd5f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00408-011-9327-y$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00408-011-9327-y$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21959954$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yao, Mengying</creatorcontrib><creatorcontrib>Zhang, Weihong</creatorcontrib><creatorcontrib>Zhang, Qingxian</creatorcontrib><creatorcontrib>Xing, Lihua</creatorcontrib><creatorcontrib>Xu, Aiguo</creatorcontrib><creatorcontrib>Liu, Qiuhong</creatorcontrib><creatorcontrib>Cui, Bing</creatorcontrib><title>Overexpression of MUC1 Enhances Proangiogenic Activity of Non-Small-Cell Lung Cancer Cells Through Activation of Akt and Extracellular Signal-regulated Kinase Pathways</title><title>Lung</title><addtitle>Lung</addtitle><addtitle>Lung</addtitle><description>Background
Angiogenesis is an important process required for tumor progression. Mucin 1 (MUC1) is a transmembrane glycoprotein that is aberrantly upregulated in many types of cancer, including non-small-cell lung cancer (NSCLC). However, the biological significance of MUC1 overexpression in lung cancer angiogenesis is not completely understood.
Methods
We showed that enforced expression of MUC1 in two NSCLC cell lines, A549 and NCI-H460, which have a low level of endogenous MUC1, promoted their ability to induce vascular endothelial growth factor (VEGF)-dependent endothelial cell migration and tube formation.
Results
There was a significant increase in VEGF expression in MUC1-overexpressing NSCLC cells. Moreover, MUC1 overexpression resulted in a marked elevation in phosphorylated Akt and extracellular signal-regulated kinase (ERK)1/2, indicative of activation of both signaling pathways. Most importantly, inhibition of Akt or ERK signaling using specific chemical inhibitors restrained the proangiogenic activity of MUC1-overexpressing NSCLC cells.
Conclusions
Taken together, our present data demonstrate that the aberrant upregulation of MUC1 favors tumor angiogenesis in NSCLC, likely through the activation of both Akt and ERK pathways and elevation of VEGF production. MUC1 may thus be a potential antiangiogenic target in NSCLC.</description><subject>Angiogenesis</subject><subject>Carcinoma, Non-Small-Cell Lung - blood supply</subject><subject>Carcinoma, Non-Small-Cell Lung - metabolism</subject><subject>Carcinoma, Non-Small-Cell Lung - pathology</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement</subject><subject>Chemical inhibitors</subject><subject>Development and progression</subject><subject>Endothelium, Vascular - metabolism</subject><subject>Endothelium, Vascular - pathology</subject><subject>Extracellular Signal-Regulated MAP Kinases - metabolism</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Glycoproteins</subject><subject>Humans</subject><subject>Lung cancer</subject><subject>Lung cancer, Non-small cell</subject><subject>Lung Neoplasms - blood supply</subject><subject>Lung Neoplasms - metabolism</subject><subject>Lung Neoplasms - pathology</subject><subject>MAP Kinase Signaling System - physiology</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mucin-1 - metabolism</subject><subject>Mucins</subject><subject>Neovascularization, Pathologic - metabolism</subject><subject>Pneumology/Respiratory System</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Signal Transduction - physiology</subject><subject>Up-Regulation</subject><subject>Vascular endothelial growth factor</subject><subject>Vascular Endothelial Growth Factor A - metabolism</subject><issn>0341-2040</issn><issn>1432-1750</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</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>eNp1ks1u1DAUhSMEotPCA7BBFkiwcvFPPEmWo2goiIFWaru2nMxN4uKxp3ZSOk_Ea-KQ4adokBeWr79zdX18kuQFJaeUkOxdICQlOSaU4oKzDO8eJTOacoZpJsjjZEZ4SjGLzFFyHMINITSbU_E0OWK0EEUh0lny_fwOPNxvPYSgnUWuQZ-vS4qWtlO2hoAuvFO21a4Fq2u0qHt9p_vdyH1xFl9ulDG4BGPQarAtKkeRR2MhoKvOu6HtJpHq9-0XX3uk7Bot73uv6ggORnl0qVurDPbQxmMPa_RJWxUAXai--6Z24VnypFEmwPP9fpJcv19elR_w6vzsY7lY4VpkrMcZZQw44ZBWVV4wAZw2c6FSUJAzxnLCi4oznldQqWhAAbXIRcrqiNB6LRp-kryd-m69ux0g9HKjwzilsuCGIAsi5nm0kUTy1T_kjRt8fMRPiFAyn7MIvZ6gVhmQ2jZufPTYUi44J3Eeno0UPkBFx8Er4yw0OpYf8KcH-LjWsNH1QcGbvwQdKNN3wZlh_JPwEKQTWHsXgodGbr3eKL-TlMgxc3LKnIyZk2Pm5C5qXu6NGKoNrH8rfoUsAmwCQryyLfg_Tv2_6w-2rOBD</recordid><startdate>20111201</startdate><enddate>20111201</enddate><creator>Yao, Mengying</creator><creator>Zhang, Weihong</creator><creator>Zhang, Qingxian</creator><creator>Xing, Lihua</creator><creator>Xu, Aiguo</creator><creator>Liu, Qiuhong</creator><creator>Cui, Bing</creator><general>Springer-Verlag</general><general>Springer</general><general>Springer Nature B.V</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>7QL</scope><scope>7RV</scope><scope>7T7</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>K9-</scope><scope>K9.</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7N</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20111201</creationdate><title>Overexpression of MUC1 Enhances Proangiogenic Activity of Non-Small-Cell Lung Cancer Cells Through Activation of Akt and Extracellular Signal-regulated Kinase Pathways</title><author>Yao, Mengying ; Zhang, Weihong ; Zhang, Qingxian ; Xing, Lihua ; Xu, Aiguo ; Liu, Qiuhong ; Cui, Bing</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c572t-7122e303e4bb8925e31f65a4eae82228039b3238beba9959ec58542c5a41cd5f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Angiogenesis</topic><topic>Carcinoma, Non-Small-Cell Lung - blood supply</topic><topic>Carcinoma, Non-Small-Cell Lung - metabolism</topic><topic>Carcinoma, Non-Small-Cell Lung - pathology</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement</topic><topic>Chemical inhibitors</topic><topic>Development and progression</topic><topic>Endothelium, Vascular - metabolism</topic><topic>Endothelium, Vascular - pathology</topic><topic>Extracellular Signal-Regulated MAP Kinases - metabolism</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Glycoproteins</topic><topic>Humans</topic><topic>Lung cancer</topic><topic>Lung cancer, Non-small cell</topic><topic>Lung Neoplasms - blood supply</topic><topic>Lung Neoplasms - metabolism</topic><topic>Lung Neoplasms - pathology</topic><topic>MAP Kinase Signaling System - physiology</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Mucin-1 - metabolism</topic><topic>Mucins</topic><topic>Neovascularization, Pathologic - metabolism</topic><topic>Pneumology/Respiratory System</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Signal Transduction - physiology</topic><topic>Up-Regulation</topic><topic>Vascular endothelial growth factor</topic><topic>Vascular Endothelial Growth Factor A - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yao, Mengying</creatorcontrib><creatorcontrib>Zhang, Weihong</creatorcontrib><creatorcontrib>Zhang, Qingxian</creatorcontrib><creatorcontrib>Xing, Lihua</creatorcontrib><creatorcontrib>Xu, Aiguo</creatorcontrib><creatorcontrib>Liu, Qiuhong</creatorcontrib><creatorcontrib>Cui, Bing</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>Bacteriology Abstracts (Microbiology B)</collection><collection>Nursing & Allied Health Database</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</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>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>Environmental Sciences and Pollution Management</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>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Consumer Health Database (Alumni Edition)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Consumer Health Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Research Library (Corporate)</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</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>MEDLINE - Academic</collection><jtitle>Lung</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yao, Mengying</au><au>Zhang, Weihong</au><au>Zhang, Qingxian</au><au>Xing, Lihua</au><au>Xu, Aiguo</au><au>Liu, Qiuhong</au><au>Cui, Bing</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Overexpression of MUC1 Enhances Proangiogenic Activity of Non-Small-Cell Lung Cancer Cells Through Activation of Akt and Extracellular Signal-regulated Kinase Pathways</atitle><jtitle>Lung</jtitle><stitle>Lung</stitle><addtitle>Lung</addtitle><date>2011-12-01</date><risdate>2011</risdate><volume>189</volume><issue>6</issue><spage>453</spage><epage>460</epage><pages>453-460</pages><issn>0341-2040</issn><eissn>1432-1750</eissn><coden>LUNGD9</coden><abstract>Background
Angiogenesis is an important process required for tumor progression. Mucin 1 (MUC1) is a transmembrane glycoprotein that is aberrantly upregulated in many types of cancer, including non-small-cell lung cancer (NSCLC). However, the biological significance of MUC1 overexpression in lung cancer angiogenesis is not completely understood.
Methods
We showed that enforced expression of MUC1 in two NSCLC cell lines, A549 and NCI-H460, which have a low level of endogenous MUC1, promoted their ability to induce vascular endothelial growth factor (VEGF)-dependent endothelial cell migration and tube formation.
Results
There was a significant increase in VEGF expression in MUC1-overexpressing NSCLC cells. Moreover, MUC1 overexpression resulted in a marked elevation in phosphorylated Akt and extracellular signal-regulated kinase (ERK)1/2, indicative of activation of both signaling pathways. Most importantly, inhibition of Akt or ERK signaling using specific chemical inhibitors restrained the proangiogenic activity of MUC1-overexpressing NSCLC cells.
Conclusions
Taken together, our present data demonstrate that the aberrant upregulation of MUC1 favors tumor angiogenesis in NSCLC, likely through the activation of both Akt and ERK pathways and elevation of VEGF production. MUC1 may thus be a potential antiangiogenic target in NSCLC.</abstract><cop>New York</cop><pub>Springer-Verlag</pub><pmid>21959954</pmid><doi>10.1007/s00408-011-9327-y</doi><tpages>8</tpages></addata></record> |
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| subjects | Angiogenesis Carcinoma, Non-Small-Cell Lung - blood supply Carcinoma, Non-Small-Cell Lung - metabolism Carcinoma, Non-Small-Cell Lung - pathology Cell Line, Tumor Cell Movement Chemical inhibitors Development and progression Endothelium, Vascular - metabolism Endothelium, Vascular - pathology Extracellular Signal-Regulated MAP Kinases - metabolism Gene Expression Regulation, Neoplastic Glycoproteins Humans Lung cancer Lung cancer, Non-small cell Lung Neoplasms - blood supply Lung Neoplasms - metabolism Lung Neoplasms - pathology MAP Kinase Signaling System - physiology Medicine Medicine & Public Health Mucin-1 - metabolism Mucins Neovascularization, Pathologic - metabolism Pneumology/Respiratory System Proto-Oncogene Proteins c-akt - metabolism Signal Transduction - physiology Up-Regulation Vascular endothelial growth factor Vascular Endothelial Growth Factor A - metabolism |
| title | Overexpression of MUC1 Enhances Proangiogenic Activity of Non-Small-Cell Lung Cancer Cells Through Activation of Akt and Extracellular Signal-regulated Kinase Pathways |
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