Frizzled2 mediates the migration and invasion of human oral squamous cell carcinoma cells through the regulation of the signal transducer and activator of transcription-3 signaling pathway
Frizzled2 (Fzd2) is a receptor for wingless-type MMTV integration site family members (Wnts), the aberrant overexpression of which has been noted to contribute to cancer metastasis. The present study was performed to characterize the role of Fzd2 in the migration and invasion of oral squamous cell c...
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| Veröffentlicht in: | Oncology reports 2015-12, Vol.34 (6), p.3061-3067 |
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| creator | ZHANG, ENJIAO LI, ZHENNING XU, ZHONGFEI DUAN, WEIYI SUN, CHANGFU LU, LI |
| description | Frizzled2 (Fzd2) is a receptor for wingless-type MMTV integration site family members (Wnts), the aberrant overexpression of which has been noted to contribute to cancer metastasis. The present study was performed to characterize the role of Fzd2 in the migration and invasion of oral squamous cell carcinomas (OSCC) in vitro. Using TSCCa cells (a tongue SCC cell line) for loss- or gain-of-function of Fzd2, we found that a forced overexpression of Fzd2 promoted TSCCa cell migration and invasion, decreased the expression of epithelial-cadherin (E-cadherin, an epithelial marker) and increased that of vimentin, Snail Slug, matrix metalloproteinases (MMPs)-2/-9/-13 and a-disintegrin and metalloproteinase with thrombospondin motifs-5 (ADAMTS5). By contrast, RNA interference (RNAi)-mediated knockdown of Fzd2 had opposite effects on OSCC cells. In addition, we found that the phosphorylation of signal transducer and activator of transcription-3 (STAT3) was enhanced by Fzd2 overexpression, but suppressed by Fzd2 depletion, and that STAT3-specific shRNA attenuated Fzd2 overexpression-induced cell invasion. In summary, the present study demonstrated that Fzd2 contributes to the migration and invasion of OSCC cells, at least partly through regulation of the STAT3 pathway. These results suggest Fzd2 as a novel therapeutic target for OSCC. |
| doi_str_mv | 10.3892/or.2015.4285 |
| format | Article |
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The present study was performed to characterize the role of Fzd2 in the migration and invasion of oral squamous cell carcinomas (OSCC) in vitro. Using TSCCa cells (a tongue SCC cell line) for loss- or gain-of-function of Fzd2, we found that a forced overexpression of Fzd2 promoted TSCCa cell migration and invasion, decreased the expression of epithelial-cadherin (E-cadherin, an epithelial marker) and increased that of vimentin, Snail Slug, matrix metalloproteinases (MMPs)-2/-9/-13 and a-disintegrin and metalloproteinase with thrombospondin motifs-5 (ADAMTS5). By contrast, RNA interference (RNAi)-mediated knockdown of Fzd2 had opposite effects on OSCC cells. In addition, we found that the phosphorylation of signal transducer and activator of transcription-3 (STAT3) was enhanced by Fzd2 overexpression, but suppressed by Fzd2 depletion, and that STAT3-specific shRNA attenuated Fzd2 overexpression-induced cell invasion. In summary, the present study demonstrated that Fzd2 contributes to the migration and invasion of OSCC cells, at least partly through regulation of the STAT3 pathway. These results suggest Fzd2 as a novel therapeutic target for OSCC.</description><identifier>ISSN: 1021-335X</identifier><identifier>EISSN: 1791-2431</identifier><identifier>DOI: 10.3892/or.2015.4285</identifier><identifier>PMID: 26398330</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Biotechnology ; Cancer ; Carcinoma, Squamous Cell - genetics ; Carcinoma, Squamous Cell - pathology ; Cell adhesion & migration ; Cell culture ; cell invasion ; Cell Line, Tumor ; cell migration ; Cell Movement - genetics ; Cell receptors ; Cellular signal transduction ; Development and progression ; Frizzled Receptors - biosynthesis ; Frizzled Receptors - genetics ; Frizzled2 ; Gene expression ; Gene Expression Regulation, Neoplastic ; Genetic aspects ; Health aspects ; Humans ; Laboratories ; Membranes ; Metastasis ; Mouth cancer ; Mouth Neoplasms - genetics ; Mouth Neoplasms - pathology ; Neoplasm Invasiveness - genetics ; Neoplasm Invasiveness - pathology ; Neoplasm Proteins - biosynthesis ; Oral cancer ; oral squamous cell carcinomas ; Plasmids ; Polyclonal antibodies ; Proteins ; signal transducer and activator of transcription-3 signaling pathway ; Signal Transduction ; Squamous cell carcinoma ; STAT3 Transcription Factor - biosynthesis ; STAT3 Transcription Factor - genetics ; Studies ; Tumorigenesis ; Tumors</subject><ispartof>Oncology reports, 2015-12, Vol.34 (6), p.3061-3067</ispartof><rights>Copyright: © Zhang et al.</rights><rights>COPYRIGHT 2015 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c486t-64124dedba1e9c78e5177ae729279d5b914831f4513cb5c6525e21a92b1e55483</citedby><cites>FETCH-LOGICAL-c486t-64124dedba1e9c78e5177ae729279d5b914831f4513cb5c6525e21a92b1e55483</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26398330$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>ZHANG, ENJIAO</creatorcontrib><creatorcontrib>LI, ZHENNING</creatorcontrib><creatorcontrib>XU, ZHONGFEI</creatorcontrib><creatorcontrib>DUAN, WEIYI</creatorcontrib><creatorcontrib>SUN, CHANGFU</creatorcontrib><creatorcontrib>LU, LI</creatorcontrib><title>Frizzled2 mediates the migration and invasion of human oral squamous cell carcinoma cells through the regulation of the signal transducer and activator of transcription-3 signaling pathway</title><title>Oncology reports</title><addtitle>Oncol Rep</addtitle><description>Frizzled2 (Fzd2) is a receptor for wingless-type MMTV integration site family members (Wnts), the aberrant overexpression of which has been noted to contribute to cancer metastasis. The present study was performed to characterize the role of Fzd2 in the migration and invasion of oral squamous cell carcinomas (OSCC) in vitro. Using TSCCa cells (a tongue SCC cell line) for loss- or gain-of-function of Fzd2, we found that a forced overexpression of Fzd2 promoted TSCCa cell migration and invasion, decreased the expression of epithelial-cadherin (E-cadherin, an epithelial marker) and increased that of vimentin, Snail Slug, matrix metalloproteinases (MMPs)-2/-9/-13 and a-disintegrin and metalloproteinase with thrombospondin motifs-5 (ADAMTS5). By contrast, RNA interference (RNAi)-mediated knockdown of Fzd2 had opposite effects on OSCC cells. In addition, we found that the phosphorylation of signal transducer and activator of transcription-3 (STAT3) was enhanced by Fzd2 overexpression, but suppressed by Fzd2 depletion, and that STAT3-specific shRNA attenuated Fzd2 overexpression-induced cell invasion. In summary, the present study demonstrated that Fzd2 contributes to the migration and invasion of OSCC cells, at least partly through regulation of the STAT3 pathway. These results suggest Fzd2 as a novel therapeutic target for OSCC.</description><subject>Biotechnology</subject><subject>Cancer</subject><subject>Carcinoma, Squamous Cell - genetics</subject><subject>Carcinoma, Squamous Cell - pathology</subject><subject>Cell adhesion & migration</subject><subject>Cell culture</subject><subject>cell invasion</subject><subject>Cell Line, Tumor</subject><subject>cell migration</subject><subject>Cell Movement - genetics</subject><subject>Cell receptors</subject><subject>Cellular signal transduction</subject><subject>Development and progression</subject><subject>Frizzled Receptors - biosynthesis</subject><subject>Frizzled Receptors - genetics</subject><subject>Frizzled2</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genetic aspects</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Laboratories</subject><subject>Membranes</subject><subject>Metastasis</subject><subject>Mouth cancer</subject><subject>Mouth Neoplasms - genetics</subject><subject>Mouth Neoplasms - pathology</subject><subject>Neoplasm Invasiveness - genetics</subject><subject>Neoplasm Invasiveness - pathology</subject><subject>Neoplasm Proteins - biosynthesis</subject><subject>Oral cancer</subject><subject>oral squamous cell carcinomas</subject><subject>Plasmids</subject><subject>Polyclonal antibodies</subject><subject>Proteins</subject><subject>signal transducer and activator of transcription-3 signaling pathway</subject><subject>Signal Transduction</subject><subject>Squamous cell carcinoma</subject><subject>STAT3 Transcription Factor - biosynthesis</subject><subject>STAT3 Transcription Factor - genetics</subject><subject>Studies</subject><subject>Tumorigenesis</subject><subject>Tumors</subject><issn>1021-335X</issn><issn>1791-2431</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNptkk1v1DAQhiMEoqVw44wiISEOZPFnEh-rigJSJS4gcYsmziRxlcRbO27V_jZ-HPbu0lKEfLA9fua1Z_xm2WtKNrxW7KN1G0ao3AhWyyfZMa0ULZjg9GlcE0YLzuXPo-yF95eEsIqU6nl2xEquas7Jcfbr3Jm7uwk7ls_YGVjR5-uI-WwGB6uxSw5Ll5vlGnza2D4fwwxx4WDK_VWA2Qafa5ymXIPTZrEz7LZJxtkwjDs5h0OY9npRIkW8GZYosTpYfBc0ut1FoFdzDat1OyydaWe2Ka_ghxSzDPkW1vEGbl9mz3qYPL46zCfZj_NP38--FBffPn89O70otKjLtSgFZaLDrgWKSlc1SlpVgBVTrFKdbBUVNae9kJTrVupSMomMgmItRSnj2Un2fq-7dfYqoF-b2fhUJCwYy29oFYVUSTmN6Nt_0EsbXHx2pBRnZc2oUA_UABM2ZultrFUn0eZU8MgRRkSkNv-h4uhwNtou2JsYf5Tw7q-EEWFaR2-nkPrnH4Mf9qB21nuHfbN1ZgZ321DSJFc11jXJVU1yVcTfHIoKbXTJPfzHRg8X-238RdNZf89YV3BRkLLgJDboN8hO1V4</recordid><startdate>20151201</startdate><enddate>20151201</enddate><creator>ZHANG, ENJIAO</creator><creator>LI, ZHENNING</creator><creator>XU, ZHONGFEI</creator><creator>DUAN, WEIYI</creator><creator>SUN, CHANGFU</creator><creator>LU, LI</creator><general>D.A. Spandidos</general><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</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>AN0</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></search><sort><creationdate>20151201</creationdate><title>Frizzled2 mediates the migration and invasion of human oral squamous cell carcinoma cells through the regulation of the signal transducer and activator of transcription-3 signaling pathway</title><author>ZHANG, ENJIAO ; LI, ZHENNING ; XU, ZHONGFEI ; DUAN, WEIYI ; SUN, CHANGFU ; LU, LI</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c486t-64124dedba1e9c78e5177ae729279d5b914831f4513cb5c6525e21a92b1e55483</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Biotechnology</topic><topic>Cancer</topic><topic>Carcinoma, Squamous Cell - genetics</topic><topic>Carcinoma, Squamous Cell - pathology</topic><topic>Cell adhesion & migration</topic><topic>Cell culture</topic><topic>cell invasion</topic><topic>Cell Line, Tumor</topic><topic>cell migration</topic><topic>Cell Movement - genetics</topic><topic>Cell receptors</topic><topic>Cellular signal transduction</topic><topic>Development and progression</topic><topic>Frizzled Receptors - biosynthesis</topic><topic>Frizzled Receptors - genetics</topic><topic>Frizzled2</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genetic aspects</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Laboratories</topic><topic>Membranes</topic><topic>Metastasis</topic><topic>Mouth cancer</topic><topic>Mouth Neoplasms - genetics</topic><topic>Mouth Neoplasms - pathology</topic><topic>Neoplasm Invasiveness - genetics</topic><topic>Neoplasm Invasiveness - pathology</topic><topic>Neoplasm Proteins - biosynthesis</topic><topic>Oral cancer</topic><topic>oral squamous cell carcinomas</topic><topic>Plasmids</topic><topic>Polyclonal antibodies</topic><topic>Proteins</topic><topic>signal transducer and activator of transcription-3 signaling pathway</topic><topic>Signal Transduction</topic><topic>Squamous cell carcinoma</topic><topic>STAT3 Transcription Factor - biosynthesis</topic><topic>STAT3 Transcription Factor - genetics</topic><topic>Studies</topic><topic>Tumorigenesis</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>ZHANG, ENJIAO</creatorcontrib><creatorcontrib>LI, ZHENNING</creatorcontrib><creatorcontrib>XU, ZHONGFEI</creatorcontrib><creatorcontrib>DUAN, WEIYI</creatorcontrib><creatorcontrib>SUN, CHANGFU</creatorcontrib><creatorcontrib>LU, LI</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>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>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><jtitle>Oncology reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>ZHANG, ENJIAO</au><au>LI, ZHENNING</au><au>XU, ZHONGFEI</au><au>DUAN, WEIYI</au><au>SUN, CHANGFU</au><au>LU, LI</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Frizzled2 mediates the migration and invasion of human oral squamous cell carcinoma cells through the regulation of the signal transducer and activator of transcription-3 signaling pathway</atitle><jtitle>Oncology reports</jtitle><addtitle>Oncol Rep</addtitle><date>2015-12-01</date><risdate>2015</risdate><volume>34</volume><issue>6</issue><spage>3061</spage><epage>3067</epage><pages>3061-3067</pages><issn>1021-335X</issn><eissn>1791-2431</eissn><abstract>Frizzled2 (Fzd2) is a receptor for wingless-type MMTV integration site family members (Wnts), the aberrant overexpression of which has been noted to contribute to cancer metastasis. The present study was performed to characterize the role of Fzd2 in the migration and invasion of oral squamous cell carcinomas (OSCC) in vitro. Using TSCCa cells (a tongue SCC cell line) for loss- or gain-of-function of Fzd2, we found that a forced overexpression of Fzd2 promoted TSCCa cell migration and invasion, decreased the expression of epithelial-cadherin (E-cadherin, an epithelial marker) and increased that of vimentin, Snail Slug, matrix metalloproteinases (MMPs)-2/-9/-13 and a-disintegrin and metalloproteinase with thrombospondin motifs-5 (ADAMTS5). By contrast, RNA interference (RNAi)-mediated knockdown of Fzd2 had opposite effects on OSCC cells. In addition, we found that the phosphorylation of signal transducer and activator of transcription-3 (STAT3) was enhanced by Fzd2 overexpression, but suppressed by Fzd2 depletion, and that STAT3-specific shRNA attenuated Fzd2 overexpression-induced cell invasion. In summary, the present study demonstrated that Fzd2 contributes to the migration and invasion of OSCC cells, at least partly through regulation of the STAT3 pathway. These results suggest Fzd2 as a novel therapeutic target for OSCC.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>26398330</pmid><doi>10.3892/or.2015.4285</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Biotechnology Cancer Carcinoma, Squamous Cell - genetics Carcinoma, Squamous Cell - pathology Cell adhesion & migration Cell culture cell invasion Cell Line, Tumor cell migration Cell Movement - genetics Cell receptors Cellular signal transduction Development and progression Frizzled Receptors - biosynthesis Frizzled Receptors - genetics Frizzled2 Gene expression Gene Expression Regulation, Neoplastic Genetic aspects Health aspects Humans Laboratories Membranes Metastasis Mouth cancer Mouth Neoplasms - genetics Mouth Neoplasms - pathology Neoplasm Invasiveness - genetics Neoplasm Invasiveness - pathology Neoplasm Proteins - biosynthesis Oral cancer oral squamous cell carcinomas Plasmids Polyclonal antibodies Proteins signal transducer and activator of transcription-3 signaling pathway Signal Transduction Squamous cell carcinoma STAT3 Transcription Factor - biosynthesis STAT3 Transcription Factor - genetics Studies Tumorigenesis Tumors |
| title | Frizzled2 mediates the migration and invasion of human oral squamous cell carcinoma cells through the regulation of the signal transducer and activator of transcription-3 signaling pathway |
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