Epithelial-mesenchymal interconversions and the regulatory function of the ZEB family during the development and progression of ovarian cancer
This study assessed the role of epithelial-mesenchymal interconversions and the regulatory functions of the ZEB family during the development and progression of ovarian cancer. E-cadherin, vimentin, ZEB1 and ZEB2 were analyzed using immunohistochemistry in a series of ovarian tissues that included n...
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| Veröffentlicht in: | Oncology letters 2016-02, Vol.11 (2), p.1463-1468 |
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| creator | WU, DI LIU, LEI REN, CHENGCHENG KONG, DAN ZHANG, PENGQI JIN, XIAOMING WANG, TIANZHEN ZHANG, GUANGMEI |
| description | This study assessed the role of epithelial-mesenchymal interconversions and the regulatory functions of the ZEB family during the development and progression of ovarian cancer. E-cadherin, vimentin, ZEB1 and ZEB2 were analyzed using immunohistochemistry in a series of ovarian tissues that included normal tissue, benign tumors, borderline tumors, malignant tumors and metastatic lesions. The correlation between E-cadherin and ZEB was analyzed. We also analyzed the association between the expression of the four factors and clinicopathological features in ovarian cancer. The results revealed that E-cadherin was weakly positive in normal ovarian epithelium. Cytoplasmic E-cadherin was significantly increased in benign tumors (P |
| doi_str_mv | 10.3892/ol.2016.4092 |
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E-cadherin, vimentin, ZEB1 and ZEB2 were analyzed using immunohistochemistry in a series of ovarian tissues that included normal tissue, benign tumors, borderline tumors, malignant tumors and metastatic lesions. The correlation between E-cadherin and ZEB was analyzed. We also analyzed the association between the expression of the four factors and clinicopathological features in ovarian cancer. The results revealed that E-cadherin was weakly positive in normal ovarian epithelium. Cytoplasmic E-cadherin was significantly increased in benign tumors (P<0.01) and further increased in borderline tumors and ovarian cancers. However, cytoplasmic E-cadherin was markedly reduced in metastatic lesions (P<0.01). Membranous E-cadherin was increased in benign tumors, but decreased progressively in borderline, malignant and metastatic tumor tissues (P<0.05). The expression profile of vimentin was opposite to that of membranous E-cadherin. Membranous E-cadherin was negatively correlated with ZEB2 expression (r=-0.514). Additionally, cytoplasmic E-cadherin, ZEB1 and ZEB2 were associated with the FIGO stage of ovarian cancer. ZEB1 was also correlated with ascitic fluid volume. Our results suggest that epithelial-mesenchymal interconversions are dynamically regulated during the development and progression of ovarian tumors. ZEB2, but not ZEB1, may regulate the expression of membranous E-cadherin during these processes.</description><identifier>ISSN: 1792-1074</identifier><identifier>EISSN: 1792-1082</identifier><identifier>DOI: 10.3892/ol.2016.4092</identifier><identifier>PMID: 26893761</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Cadherins ; Cancer therapies ; Cell adhesion & migration ; Cysts ; Cytoplasm ; Development and progression ; EMT ; Gene expression ; Genetic aspects ; Health aspects ; Immunoglobulins ; MET ; Metastasis ; Oncology ; Ovarian cancer ; Regulation ; Studies ; Transcription factors ; Tumors ; ZEB1 ; ZEB2</subject><ispartof>Oncology letters, 2016-02, Vol.11 (2), p.1463-1468</ispartof><rights>Copyright © 2016, Spandidos Publications</rights><rights>COPYRIGHT 2016 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2016</rights><rights>Copyright © 2016, Spandidos Publications 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c605t-c5fd0c9ad5f8fa968380a95004f5f8a86d04d2d58fd8e2c4a4c15564419870bd3</citedby><cites>FETCH-LOGICAL-c605t-c5fd0c9ad5f8fa968380a95004f5f8a86d04d2d58fd8e2c4a4c15564419870bd3</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/PMC4734304/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4734304/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,315,728,781,785,886,5573,27929,27930,53796,53798</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26893761$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>WU, DI</creatorcontrib><creatorcontrib>LIU, LEI</creatorcontrib><creatorcontrib>REN, CHENGCHENG</creatorcontrib><creatorcontrib>KONG, DAN</creatorcontrib><creatorcontrib>ZHANG, PENGQI</creatorcontrib><creatorcontrib>JIN, XIAOMING</creatorcontrib><creatorcontrib>WANG, TIANZHEN</creatorcontrib><creatorcontrib>ZHANG, GUANGMEI</creatorcontrib><title>Epithelial-mesenchymal interconversions and the regulatory function of the ZEB family during the development and progression of ovarian cancer</title><title>Oncology letters</title><addtitle>Oncol Lett</addtitle><description>This study assessed the role of epithelial-mesenchymal interconversions and the regulatory functions of the ZEB family during the development and progression of ovarian cancer. E-cadherin, vimentin, ZEB1 and ZEB2 were analyzed using immunohistochemistry in a series of ovarian tissues that included normal tissue, benign tumors, borderline tumors, malignant tumors and metastatic lesions. The correlation between E-cadherin and ZEB was analyzed. We also analyzed the association between the expression of the four factors and clinicopathological features in ovarian cancer. The results revealed that E-cadherin was weakly positive in normal ovarian epithelium. Cytoplasmic E-cadherin was significantly increased in benign tumors (P<0.01) and further increased in borderline tumors and ovarian cancers. However, cytoplasmic E-cadherin was markedly reduced in metastatic lesions (P<0.01). Membranous E-cadherin was increased in benign tumors, but decreased progressively in borderline, malignant and metastatic tumor tissues (P<0.05). The expression profile of vimentin was opposite to that of membranous E-cadherin. Membranous E-cadherin was negatively correlated with ZEB2 expression (r=-0.514). Additionally, cytoplasmic E-cadherin, ZEB1 and ZEB2 were associated with the FIGO stage of ovarian cancer. ZEB1 was also correlated with ascitic fluid volume. Our results suggest that epithelial-mesenchymal interconversions are dynamically regulated during the development and progression of ovarian tumors. ZEB2, but not ZEB1, may regulate the expression of membranous E-cadherin during these processes.</description><subject>Cadherins</subject><subject>Cancer therapies</subject><subject>Cell adhesion & migration</subject><subject>Cysts</subject><subject>Cytoplasm</subject><subject>Development and progression</subject><subject>EMT</subject><subject>Gene expression</subject><subject>Genetic aspects</subject><subject>Health aspects</subject><subject>Immunoglobulins</subject><subject>MET</subject><subject>Metastasis</subject><subject>Oncology</subject><subject>Ovarian cancer</subject><subject>Regulation</subject><subject>Studies</subject><subject>Transcription factors</subject><subject>Tumors</subject><subject>ZEB1</subject><subject>ZEB2</subject><issn>1792-1074</issn><issn>1792-1082</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNptkk1v1DAQhiMEolXpjTOKBEIcyGInjuNckEq1fEgr9QIXLpZrj7OuHDvYyUr7J_jNOLtL1EV4DrZmnnltz0yWvcRoVbG2_ODtqkSYrghqyyfZJW7assCIlU-Xc0MususYH1BaNcWM0efZRUlZWzUUX2a_14MZt2CNsEUPEZzc7nthc-NGCNK7HYRovIu5cCpPYB6gm6wYfdjnenJyTMHc60Po5_pTrkVv7D5XUzCuO3gV7MD6oQc3HkSG4LsAMZ4S_U4EI1wuhZMQXmTPtLARrk_7Vfbj8_r77ddic_fl2-3NppAU1WMha62QbIWqNdOipaxiSLQ1QkQnj2BUIaJKVTOtGJSSCCJxXVNCcMsadK-qq-zjUXeY7ntQMj0uCMuHYHoR9twLw88jzmx553ecNBWpEEkC704Cwf-aII68N1GCtcKBnyLHrKQ01ZtWCX39D_rgp-DS9zhuq5ISStMHFqoTFrhx2qd75SzKbwhpaMVIVSdq9R8qmYLepHaBNsl_lvD2UcIWhB230dtp7ls8B98fQRl8jAH0UgyM-Dxr3Fs-zxqfZy3hrx4XcIH_TlYC3hyBOKSuG-XjwtxtCpTsoPMHl5vcZQ</recordid><startdate>20160201</startdate><enddate>20160201</enddate><creator>WU, DI</creator><creator>LIU, LEI</creator><creator>REN, CHENGCHENG</creator><creator>KONG, DAN</creator><creator>ZHANG, PENGQI</creator><creator>JIN, XIAOMING</creator><creator>WANG, TIANZHEN</creator><creator>ZHANG, GUANGMEI</creator><general>D.A. Spandidos</general><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20160201</creationdate><title>Epithelial-mesenchymal interconversions and the regulatory function of the ZEB family during the development and progression of ovarian cancer</title><author>WU, DI ; LIU, LEI ; REN, CHENGCHENG ; KONG, DAN ; ZHANG, PENGQI ; JIN, XIAOMING ; WANG, TIANZHEN ; ZHANG, GUANGMEI</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c605t-c5fd0c9ad5f8fa968380a95004f5f8a86d04d2d58fd8e2c4a4c15564419870bd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Cadherins</topic><topic>Cancer therapies</topic><topic>Cell adhesion & migration</topic><topic>Cysts</topic><topic>Cytoplasm</topic><topic>Development and progression</topic><topic>EMT</topic><topic>Gene expression</topic><topic>Genetic aspects</topic><topic>Health aspects</topic><topic>Immunoglobulins</topic><topic>MET</topic><topic>Metastasis</topic><topic>Oncology</topic><topic>Ovarian cancer</topic><topic>Regulation</topic><topic>Studies</topic><topic>Transcription factors</topic><topic>Tumors</topic><topic>ZEB1</topic><topic>ZEB2</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>WU, DI</creatorcontrib><creatorcontrib>LIU, LEI</creatorcontrib><creatorcontrib>REN, CHENGCHENG</creatorcontrib><creatorcontrib>KONG, DAN</creatorcontrib><creatorcontrib>ZHANG, PENGQI</creatorcontrib><creatorcontrib>JIN, XIAOMING</creatorcontrib><creatorcontrib>WANG, TIANZHEN</creatorcontrib><creatorcontrib>ZHANG, GUANGMEI</creatorcontrib><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>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>British Nursing Database</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>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>Oncology letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>WU, DI</au><au>LIU, LEI</au><au>REN, CHENGCHENG</au><au>KONG, DAN</au><au>ZHANG, PENGQI</au><au>JIN, XIAOMING</au><au>WANG, TIANZHEN</au><au>ZHANG, GUANGMEI</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Epithelial-mesenchymal interconversions and the regulatory function of the ZEB family during the development and progression of ovarian cancer</atitle><jtitle>Oncology letters</jtitle><addtitle>Oncol Lett</addtitle><date>2016-02-01</date><risdate>2016</risdate><volume>11</volume><issue>2</issue><spage>1463</spage><epage>1468</epage><pages>1463-1468</pages><issn>1792-1074</issn><eissn>1792-1082</eissn><abstract>This study assessed the role of epithelial-mesenchymal interconversions and the regulatory functions of the ZEB family during the development and progression of ovarian cancer. E-cadherin, vimentin, ZEB1 and ZEB2 were analyzed using immunohistochemistry in a series of ovarian tissues that included normal tissue, benign tumors, borderline tumors, malignant tumors and metastatic lesions. The correlation between E-cadherin and ZEB was analyzed. We also analyzed the association between the expression of the four factors and clinicopathological features in ovarian cancer. The results revealed that E-cadherin was weakly positive in normal ovarian epithelium. Cytoplasmic E-cadherin was significantly increased in benign tumors (P<0.01) and further increased in borderline tumors and ovarian cancers. However, cytoplasmic E-cadherin was markedly reduced in metastatic lesions (P<0.01). Membranous E-cadherin was increased in benign tumors, but decreased progressively in borderline, malignant and metastatic tumor tissues (P<0.05). The expression profile of vimentin was opposite to that of membranous E-cadherin. Membranous E-cadherin was negatively correlated with ZEB2 expression (r=-0.514). Additionally, cytoplasmic E-cadherin, ZEB1 and ZEB2 were associated with the FIGO stage of ovarian cancer. ZEB1 was also correlated with ascitic fluid volume. Our results suggest that epithelial-mesenchymal interconversions are dynamically regulated during the development and progression of ovarian tumors. ZEB2, but not ZEB1, may regulate the expression of membranous E-cadherin during these processes.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>26893761</pmid><doi>10.3892/ol.2016.4092</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1792-1074 |
| ispartof | Oncology letters, 2016-02, Vol.11 (2), p.1463-1468 |
| issn | 1792-1074 1792-1082 |
| language | eng |
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| source | Spandidos Publications Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
| subjects | Cadherins Cancer therapies Cell adhesion & migration Cysts Cytoplasm Development and progression EMT Gene expression Genetic aspects Health aspects Immunoglobulins MET Metastasis Oncology Ovarian cancer Regulation Studies Transcription factors Tumors ZEB1 ZEB2 |
| title | Epithelial-mesenchymal interconversions and the regulatory function of the ZEB family during the development and progression of ovarian cancer |
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