MTA1-upregulated EpCAM is associated with metastatic behaviors and poor prognosis in lung cancer
Overexpression of Metastasis-associated protein 1 (MTA1) in various cancer cells promotes tumor invasion and migration and predicts cancer patients' poor prognosis. The pilot RNA-Seq data from our laboratory indicated that Epithelial cell adhesion molecule (EpCAM) was statistically reduced in M...
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| Veröffentlicht in: | Journal of experimental & clinical cancer research 2015-12, Vol.34 (156), p.157-157, Article 157 |
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| creator | Zhou, Ning Wang, Haijuan Liu, Hongxu Xue, Hongsheng Lin, Feng Meng, Xiting Liang, Ailing Zhao, Zhilong Liu, YongJun Qian, Haili |
| description | Overexpression of Metastasis-associated protein 1 (MTA1) in various cancer cells promotes tumor invasion and migration and predicts cancer patients' poor prognosis. The pilot RNA-Seq data from our laboratory indicated that Epithelial cell adhesion molecule (EpCAM) was statistically reduced in MTA1-silencing cells. EpCAM has been recognized as more than a mere cell adhesion molecule and recent findings have revealed its causal role in mediating migratory and invasive capacity. Thus, this study was aimed to explore whether MTA1 was able to upregulate EpCAM expression and, consequently, modulate its effects on invasion and migration of the lung cancer cells as well as patients' prognosis.
We checked the EpCAM expression by overexpressing or silencing MTA1 in lung cancer cells. Furthermore, these lung cancer cells with stably overexpressed or silenced MTA1 were transfected with siEpCAM or EpCAM-expressing plasmids and then subjected to western blot, invasion and migration assays. In addition, patients (n = 118) with early-stage lung cancer were enrolled in this study to confirm the correlations between MTA1 and EpCAM and pathoclinical parameters by using immunohistochemistry (IHC). All statistical analyses were performed with SPSS 20.0 statistical software.
MTA1 upregulated EpCAM expression in lung cancer cell lines, and EpCAM overexpression rescued the inhibitory effects by silencing MTA1 on cell invasion and migration in vitro. What's more, both MTA1 and EpCAM, correlated to each other, were overexpressed in lung cancer tissues and significantly correlated with their clinical stages, tumor diameters, lymph node metastasis. Multivariate analysis indicated that local advancement (p = 0.03), MTA1 overexpression (p = 0.001) and EpCAM overexpression (p = 0.045) of the lung cancer tissues remained significant in predicting unfavorable overall survival.
We revealed a new molecular mechanism of MTA1-mediated invasion and metastasis in lung cancer through downstream target EpCAM, and interfering with EpCAM function may be a novel therapeutic strategy for treatment of MTA1-overexpressing lung carcinoma. |
| doi_str_mv | 10.1186/s13046-015-0263-1 |
| format | Article |
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We checked the EpCAM expression by overexpressing or silencing MTA1 in lung cancer cells. Furthermore, these lung cancer cells with stably overexpressed or silenced MTA1 were transfected with siEpCAM or EpCAM-expressing plasmids and then subjected to western blot, invasion and migration assays. In addition, patients (n = 118) with early-stage lung cancer were enrolled in this study to confirm the correlations between MTA1 and EpCAM and pathoclinical parameters by using immunohistochemistry (IHC). All statistical analyses were performed with SPSS 20.0 statistical software.
MTA1 upregulated EpCAM expression in lung cancer cell lines, and EpCAM overexpression rescued the inhibitory effects by silencing MTA1 on cell invasion and migration in vitro. What's more, both MTA1 and EpCAM, correlated to each other, were overexpressed in lung cancer tissues and significantly correlated with their clinical stages, tumor diameters, lymph node metastasis. Multivariate analysis indicated that local advancement (p = 0.03), MTA1 overexpression (p = 0.001) and EpCAM overexpression (p = 0.045) of the lung cancer tissues remained significant in predicting unfavorable overall survival.
We revealed a new molecular mechanism of MTA1-mediated invasion and metastasis in lung cancer through downstream target EpCAM, and interfering with EpCAM function may be a novel therapeutic strategy for treatment of MTA1-overexpressing lung carcinoma.</description><identifier>ISSN: 1756-9966</identifier><identifier>ISSN: 0392-9078</identifier><identifier>EISSN: 1756-9966</identifier><identifier>DOI: 10.1186/s13046-015-0263-1</identifier><identifier>PMID: 26698569</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Adult ; Analysis ; Antigens, Neoplasm - biosynthesis ; Antigens, Neoplasm - genetics ; Care and treatment ; Cell Adhesion Molecules - biosynthesis ; Cell Adhesion Molecules - genetics ; Cell Line, Tumor ; Cell Movement - genetics ; Cell Proliferation - genetics ; Complications and side effects ; Epithelial Cell Adhesion Molecule ; Female ; Gene Expression Regulation, Neoplastic ; Histone Deacetylases - biosynthesis ; Histone Deacetylases - genetics ; Humans ; Immunohistochemistry ; Lung cancer ; Lung Neoplasms - genetics ; Lung Neoplasms - pathology ; Lymphatic Metastasis ; Male ; Metastasis ; Middle Aged ; Neoplasm Invasiveness - genetics ; Prognosis ; Repressor Proteins - antagonists & inhibitors ; Repressor Proteins - biosynthesis ; Repressor Proteins - genetics ; Risk factors ; RNA sequencing ; Trans-Activators</subject><ispartof>Journal of experimental & clinical cancer research, 2015-12, Vol.34 (156), p.157-157, Article 157</ispartof><rights>COPYRIGHT 2015 BioMed Central Ltd.</rights><rights>Copyright BioMed Central 2015</rights><rights>Zhou et al. 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c573t-d937fce49b957d6eaa9f7248b702152f44ceaea8a7ba7162f5fb04e9624788933</citedby><cites>FETCH-LOGICAL-c573t-d937fce49b957d6eaa9f7248b702152f44ceaea8a7ba7162f5fb04e9624788933</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/PMC4690245/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4690245/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,27915,27916,53782,53784</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26698569$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhou, Ning</creatorcontrib><creatorcontrib>Wang, Haijuan</creatorcontrib><creatorcontrib>Liu, Hongxu</creatorcontrib><creatorcontrib>Xue, Hongsheng</creatorcontrib><creatorcontrib>Lin, Feng</creatorcontrib><creatorcontrib>Meng, Xiting</creatorcontrib><creatorcontrib>Liang, Ailing</creatorcontrib><creatorcontrib>Zhao, Zhilong</creatorcontrib><creatorcontrib>Liu, YongJun</creatorcontrib><creatorcontrib>Qian, Haili</creatorcontrib><title>MTA1-upregulated EpCAM is associated with metastatic behaviors and poor prognosis in lung cancer</title><title>Journal of experimental & clinical cancer research</title><addtitle>J Exp Clin Cancer Res</addtitle><description>Overexpression of Metastasis-associated protein 1 (MTA1) in various cancer cells promotes tumor invasion and migration and predicts cancer patients' poor prognosis. The pilot RNA-Seq data from our laboratory indicated that Epithelial cell adhesion molecule (EpCAM) was statistically reduced in MTA1-silencing cells. EpCAM has been recognized as more than a mere cell adhesion molecule and recent findings have revealed its causal role in mediating migratory and invasive capacity. Thus, this study was aimed to explore whether MTA1 was able to upregulate EpCAM expression and, consequently, modulate its effects on invasion and migration of the lung cancer cells as well as patients' prognosis.
We checked the EpCAM expression by overexpressing or silencing MTA1 in lung cancer cells. Furthermore, these lung cancer cells with stably overexpressed or silenced MTA1 were transfected with siEpCAM or EpCAM-expressing plasmids and then subjected to western blot, invasion and migration assays. In addition, patients (n = 118) with early-stage lung cancer were enrolled in this study to confirm the correlations between MTA1 and EpCAM and pathoclinical parameters by using immunohistochemistry (IHC). All statistical analyses were performed with SPSS 20.0 statistical software.
MTA1 upregulated EpCAM expression in lung cancer cell lines, and EpCAM overexpression rescued the inhibitory effects by silencing MTA1 on cell invasion and migration in vitro. What's more, both MTA1 and EpCAM, correlated to each other, were overexpressed in lung cancer tissues and significantly correlated with their clinical stages, tumor diameters, lymph node metastasis. Multivariate analysis indicated that local advancement (p = 0.03), MTA1 overexpression (p = 0.001) and EpCAM overexpression (p = 0.045) of the lung cancer tissues remained significant in predicting unfavorable overall survival.
We revealed a new molecular mechanism of MTA1-mediated invasion and metastasis in lung cancer through downstream target EpCAM, and interfering with EpCAM function may be a novel therapeutic strategy for treatment of MTA1-overexpressing lung carcinoma.</description><subject>Adult</subject><subject>Analysis</subject><subject>Antigens, Neoplasm - biosynthesis</subject><subject>Antigens, Neoplasm - genetics</subject><subject>Care and treatment</subject><subject>Cell Adhesion Molecules - biosynthesis</subject><subject>Cell Adhesion Molecules - genetics</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement - genetics</subject><subject>Cell Proliferation - genetics</subject><subject>Complications and side effects</subject><subject>Epithelial Cell Adhesion Molecule</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Histone Deacetylases - biosynthesis</subject><subject>Histone Deacetylases - genetics</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Lung cancer</subject><subject>Lung Neoplasms - genetics</subject><subject>Lung Neoplasms - pathology</subject><subject>Lymphatic Metastasis</subject><subject>Male</subject><subject>Metastasis</subject><subject>Middle Aged</subject><subject>Neoplasm Invasiveness - genetics</subject><subject>Prognosis</subject><subject>Repressor Proteins - antagonists & inhibitors</subject><subject>Repressor Proteins - biosynthesis</subject><subject>Repressor Proteins - genetics</subject><subject>Risk factors</subject><subject>RNA sequencing</subject><subject>Trans-Activators</subject><issn>1756-9966</issn><issn>0392-9078</issn><issn>1756-9966</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><recordid>eNptkktv1DAUhSMEoqXwA9igSEiITYrt-BFvkEaj8pBasSlr4zg3iavEDrZTxL_H0xmqGYS8sHX9nWP53lMUrzG6xLjhHyKuEeUVwqxChNcVflKcY8F4JSXnT4_OZ8WLGO8Q4lhi-bw4I5zLhnF5Xvy4ud3gal0CDOukE3Tl1bLd3JQ2ljpGb-xD7ZdNYzlD0jHpZE3ZwqjvrQ8Zcl25eB_KJfjB-Zh11pXT6obSaGcgvCye9XqK8OqwXxTfP13dbr9U198-f91urivDRJ2qTtaiN0BlK5noOGgte0Fo0wpEMCM9pQY06EaLVgvMSc_6FlGQnFDRNLKuL4qPe99lbWfoDLgU9KSWYGcdfiuvrTq9cXZUg79XlEtEKMsG7w8Gwf9cISY122hgmrQDv0aVm0lqhhuMMvr2H_TOr8Hl72VKSJ6H82B4oAY9gbKu9_ldszNVG8pwHgElTaYu_0Pl1cFsjXfQ21w_Ebw7EoygpzRGP63JehdPQbwHTfAxBugfm4GR2uVH7fOjcn7ULj8KZ82b4y4-Kv4Gpv4Dpum_Kw</recordid><startdate>20151223</startdate><enddate>20151223</enddate><creator>Zhou, Ning</creator><creator>Wang, Haijuan</creator><creator>Liu, Hongxu</creator><creator>Xue, Hongsheng</creator><creator>Lin, Feng</creator><creator>Meng, Xiting</creator><creator>Liang, Ailing</creator><creator>Zhao, Zhilong</creator><creator>Liu, YongJun</creator><creator>Qian, Haili</creator><general>BioMed Central Ltd</general><general>BioMed Central</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></search><sort><creationdate>20151223</creationdate><title>MTA1-upregulated EpCAM is associated with metastatic behaviors and poor prognosis in lung cancer</title><author>Zhou, Ning ; Wang, Haijuan ; Liu, Hongxu ; Xue, Hongsheng ; Lin, Feng ; Meng, Xiting ; Liang, Ailing ; Zhao, Zhilong ; Liu, YongJun ; Qian, Haili</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c573t-d937fce49b957d6eaa9f7248b702152f44ceaea8a7ba7162f5fb04e9624788933</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Adult</topic><topic>Analysis</topic><topic>Antigens, Neoplasm - biosynthesis</topic><topic>Antigens, Neoplasm - genetics</topic><topic>Care and treatment</topic><topic>Cell Adhesion Molecules - biosynthesis</topic><topic>Cell Adhesion Molecules - genetics</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement - genetics</topic><topic>Cell Proliferation - genetics</topic><topic>Complications and side effects</topic><topic>Epithelial Cell Adhesion Molecule</topic><topic>Female</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Histone Deacetylases - biosynthesis</topic><topic>Histone Deacetylases - genetics</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Lung cancer</topic><topic>Lung Neoplasms - genetics</topic><topic>Lung Neoplasms - pathology</topic><topic>Lymphatic Metastasis</topic><topic>Male</topic><topic>Metastasis</topic><topic>Middle Aged</topic><topic>Neoplasm Invasiveness - genetics</topic><topic>Prognosis</topic><topic>Repressor Proteins - antagonists & inhibitors</topic><topic>Repressor Proteins - biosynthesis</topic><topic>Repressor Proteins - genetics</topic><topic>Risk factors</topic><topic>RNA sequencing</topic><topic>Trans-Activators</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhou, Ning</creatorcontrib><creatorcontrib>Wang, Haijuan</creatorcontrib><creatorcontrib>Liu, Hongxu</creatorcontrib><creatorcontrib>Xue, Hongsheng</creatorcontrib><creatorcontrib>Lin, Feng</creatorcontrib><creatorcontrib>Meng, Xiting</creatorcontrib><creatorcontrib>Liang, Ailing</creatorcontrib><creatorcontrib>Zhao, Zhilong</creatorcontrib><creatorcontrib>Liu, YongJun</creatorcontrib><creatorcontrib>Qian, Haili</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>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 Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</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>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><jtitle>Journal of experimental & clinical cancer research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhou, Ning</au><au>Wang, Haijuan</au><au>Liu, Hongxu</au><au>Xue, Hongsheng</au><au>Lin, Feng</au><au>Meng, Xiting</au><au>Liang, Ailing</au><au>Zhao, Zhilong</au><au>Liu, YongJun</au><au>Qian, Haili</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MTA1-upregulated EpCAM is associated with metastatic behaviors and poor prognosis in lung cancer</atitle><jtitle>Journal of experimental & clinical cancer research</jtitle><addtitle>J Exp Clin Cancer Res</addtitle><date>2015-12-23</date><risdate>2015</risdate><volume>34</volume><issue>156</issue><spage>157</spage><epage>157</epage><pages>157-157</pages><artnum>157</artnum><issn>1756-9966</issn><issn>0392-9078</issn><eissn>1756-9966</eissn><abstract>Overexpression of Metastasis-associated protein 1 (MTA1) in various cancer cells promotes tumor invasion and migration and predicts cancer patients' poor prognosis. The pilot RNA-Seq data from our laboratory indicated that Epithelial cell adhesion molecule (EpCAM) was statistically reduced in MTA1-silencing cells. EpCAM has been recognized as more than a mere cell adhesion molecule and recent findings have revealed its causal role in mediating migratory and invasive capacity. Thus, this study was aimed to explore whether MTA1 was able to upregulate EpCAM expression and, consequently, modulate its effects on invasion and migration of the lung cancer cells as well as patients' prognosis.
We checked the EpCAM expression by overexpressing or silencing MTA1 in lung cancer cells. Furthermore, these lung cancer cells with stably overexpressed or silenced MTA1 were transfected with siEpCAM or EpCAM-expressing plasmids and then subjected to western blot, invasion and migration assays. In addition, patients (n = 118) with early-stage lung cancer were enrolled in this study to confirm the correlations between MTA1 and EpCAM and pathoclinical parameters by using immunohistochemistry (IHC). All statistical analyses were performed with SPSS 20.0 statistical software.
MTA1 upregulated EpCAM expression in lung cancer cell lines, and EpCAM overexpression rescued the inhibitory effects by silencing MTA1 on cell invasion and migration in vitro. What's more, both MTA1 and EpCAM, correlated to each other, were overexpressed in lung cancer tissues and significantly correlated with their clinical stages, tumor diameters, lymph node metastasis. Multivariate analysis indicated that local advancement (p = 0.03), MTA1 overexpression (p = 0.001) and EpCAM overexpression (p = 0.045) of the lung cancer tissues remained significant in predicting unfavorable overall survival.
We revealed a new molecular mechanism of MTA1-mediated invasion and metastasis in lung cancer through downstream target EpCAM, and interfering with EpCAM function may be a novel therapeutic strategy for treatment of MTA1-overexpressing lung carcinoma.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>26698569</pmid><doi>10.1186/s13046-015-0263-1</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adult Analysis Antigens, Neoplasm - biosynthesis Antigens, Neoplasm - genetics Care and treatment Cell Adhesion Molecules - biosynthesis Cell Adhesion Molecules - genetics Cell Line, Tumor Cell Movement - genetics Cell Proliferation - genetics Complications and side effects Epithelial Cell Adhesion Molecule Female Gene Expression Regulation, Neoplastic Histone Deacetylases - biosynthesis Histone Deacetylases - genetics Humans Immunohistochemistry Lung cancer Lung Neoplasms - genetics Lung Neoplasms - pathology Lymphatic Metastasis Male Metastasis Middle Aged Neoplasm Invasiveness - genetics Prognosis Repressor Proteins - antagonists & inhibitors Repressor Proteins - biosynthesis Repressor Proteins - genetics Risk factors RNA sequencing Trans-Activators |
| title | MTA1-upregulated EpCAM is associated with metastatic behaviors and poor prognosis in lung cancer |
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