High FMNL3 expression promotes nasopharyngeal carcinoma cell metastasis: role in TGF-β1-induced epithelia-to-mesenchymal transition
Formin-like 3 (FMNL3) plays a crucial role in cytoskeletal mediation and is potentially a biomarker for cell migration; however, its role in cancer metastasis remains unknown. In this study, we found elevated FMNL3 protein expression in clinical nasopharyngeal carcinoma (NPC) tissues. FMNL3 expressi...
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| creator | Wu, Yanxia Shen, Zhihua Wang, Keke Ha, Yanping Lei, Hong Jia, Yanan Ding, Ranran Wu, Dongmei Gan, Siyuan Li, Rujia Luo, Botao Jiang, Hanguo Jie, Wei |
| description | Formin-like 3 (FMNL3) plays a crucial role in cytoskeletal mediation and is potentially a biomarker for cell migration; however, its role in cancer metastasis remains unknown. In this study, we found elevated FMNL3 protein expression in clinical nasopharyngeal carcinoma (NPC) tissues. FMNL3 expression positively correlated to the clinical stage, T (tumour), N (lymph node metastasis) and M (distant metastasis) classification of NPC patients. Moreover, FMNL3 positively correlated to Vimentin expression and negatively correlated to E-cadherin expression in clinical NPC samples.
In vitro
experiments showed that FMNL3 expression was inversely related to NPC cell differentiation status. Overexpression of FMNL3 led to epithelial-to-mesenchymal transition (EMT) in well differentiated CNE1 cells. TGF-β1-treated poorly differentiated CNE2 cells showed changes in EMT accompanied by enhanced FMNL3 expression and cell migration. On the contrary, knockdown of FMNL3 partially attenuated the TGF-β1-promoted CNE2 cell migration, together with associated changes in EMT markers. Finally, knockdown of FMNL3 also weakened EMT in tumours in xenographs. Our study indicates for the first time that TGF-β1/FMNL3 signalling may be a novel mechanism mediating EMT in NPC, which is closely associated with NPC metastasis. |
| doi_str_mv | 10.1038/srep42507 |
| format | Article |
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In vitro
experiments showed that FMNL3 expression was inversely related to NPC cell differentiation status. Overexpression of FMNL3 led to epithelial-to-mesenchymal transition (EMT) in well differentiated CNE1 cells. TGF-β1-treated poorly differentiated CNE2 cells showed changes in EMT accompanied by enhanced FMNL3 expression and cell migration. On the contrary, knockdown of FMNL3 partially attenuated the TGF-β1-promoted CNE2 cell migration, together with associated changes in EMT markers. Finally, knockdown of FMNL3 also weakened EMT in tumours in xenographs. Our study indicates for the first time that TGF-β1/FMNL3 signalling may be a novel mechanism mediating EMT in NPC, which is closely associated with NPC metastasis.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/srep42507</identifier><identifier>PMID: 28198387</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/109 ; 13/89 ; 14/19 ; 38/77 ; 64/60 ; 692/4028/67/322 ; 692/420/755 ; 82 ; 82/80 ; Adult ; Aged ; Biomarkers ; Cadherins - metabolism ; Carcinoma - genetics ; Carcinoma - metabolism ; Carcinoma - pathology ; Cell adhesion & migration ; Cell differentiation ; Cell Line, Tumor ; Cell migration ; Cell Movement ; Cytoskeleton ; E-cadherin ; Epithelial-Mesenchymal Transition - drug effects ; Epithelial-Mesenchymal Transition - genetics ; Female ; Formins ; Gene Expression ; Humanities and Social Sciences ; Humans ; Immunohistochemistry ; Lymph nodes ; Male ; Mesenchyme ; Metastases ; Metastasis ; Middle Aged ; multidisciplinary ; Nasopharyngeal Carcinoma ; Nasopharyngeal Neoplasms - genetics ; Nasopharyngeal Neoplasms - metabolism ; Nasopharyngeal Neoplasms - pathology ; Proteins - genetics ; Proteins - metabolism ; Science ; Throat cancer ; Transforming Growth Factor beta1 - metabolism ; Transforming growth factor-b1 ; Tumors ; Vimentin ; Vimentin - metabolism</subject><ispartof>Scientific reports, 2017-02, Vol.7 (1), p.42507-42507, Article 42507</ispartof><rights>The Author(s) 2017</rights><rights>The Author(s) 2017. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Copyright © 2017, The Author(s) 2017 The Author(s)</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c504t-43627b7d28ee5e55437fe64cf146c4cac4fb1b9d77653c8ab2cbafbc92eb6f1d3</citedby><cites>FETCH-LOGICAL-c504t-43627b7d28ee5e55437fe64cf146c4cac4fb1b9d77653c8ab2cbafbc92eb6f1d3</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/PMC5309845/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5309845/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,865,886,27929,27930,41125,42194,51581,53796,53798</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28198387$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wu, Yanxia</creatorcontrib><creatorcontrib>Shen, Zhihua</creatorcontrib><creatorcontrib>Wang, Keke</creatorcontrib><creatorcontrib>Ha, Yanping</creatorcontrib><creatorcontrib>Lei, Hong</creatorcontrib><creatorcontrib>Jia, Yanan</creatorcontrib><creatorcontrib>Ding, Ranran</creatorcontrib><creatorcontrib>Wu, Dongmei</creatorcontrib><creatorcontrib>Gan, Siyuan</creatorcontrib><creatorcontrib>Li, Rujia</creatorcontrib><creatorcontrib>Luo, Botao</creatorcontrib><creatorcontrib>Jiang, Hanguo</creatorcontrib><creatorcontrib>Jie, Wei</creatorcontrib><title>High FMNL3 expression promotes nasopharyngeal carcinoma cell metastasis: role in TGF-β1-induced epithelia-to-mesenchymal transition</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>Formin-like 3 (FMNL3) plays a crucial role in cytoskeletal mediation and is potentially a biomarker for cell migration; however, its role in cancer metastasis remains unknown. In this study, we found elevated FMNL3 protein expression in clinical nasopharyngeal carcinoma (NPC) tissues. FMNL3 expression positively correlated to the clinical stage, T (tumour), N (lymph node metastasis) and M (distant metastasis) classification of NPC patients. Moreover, FMNL3 positively correlated to Vimentin expression and negatively correlated to E-cadherin expression in clinical NPC samples.
In vitro
experiments showed that FMNL3 expression was inversely related to NPC cell differentiation status. Overexpression of FMNL3 led to epithelial-to-mesenchymal transition (EMT) in well differentiated CNE1 cells. TGF-β1-treated poorly differentiated CNE2 cells showed changes in EMT accompanied by enhanced FMNL3 expression and cell migration. On the contrary, knockdown of FMNL3 partially attenuated the TGF-β1-promoted CNE2 cell migration, together with associated changes in EMT markers. Finally, knockdown of FMNL3 also weakened EMT in tumours in xenographs. Our study indicates for the first time that TGF-β1/FMNL3 signalling may be a novel mechanism mediating EMT in NPC, which is closely associated with NPC metastasis.</description><subject>13/109</subject><subject>13/89</subject><subject>14/19</subject><subject>38/77</subject><subject>64/60</subject><subject>692/4028/67/322</subject><subject>692/420/755</subject><subject>82</subject><subject>82/80</subject><subject>Adult</subject><subject>Aged</subject><subject>Biomarkers</subject><subject>Cadherins - metabolism</subject><subject>Carcinoma - genetics</subject><subject>Carcinoma - metabolism</subject><subject>Carcinoma - pathology</subject><subject>Cell adhesion & migration</subject><subject>Cell differentiation</subject><subject>Cell Line, Tumor</subject><subject>Cell migration</subject><subject>Cell Movement</subject><subject>Cytoskeleton</subject><subject>E-cadherin</subject><subject>Epithelial-Mesenchymal Transition - drug effects</subject><subject>Epithelial-Mesenchymal Transition - genetics</subject><subject>Female</subject><subject>Formins</subject><subject>Gene Expression</subject><subject>Humanities and Social Sciences</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Lymph nodes</subject><subject>Male</subject><subject>Mesenchyme</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>Middle Aged</subject><subject>multidisciplinary</subject><subject>Nasopharyngeal Carcinoma</subject><subject>Nasopharyngeal Neoplasms - genetics</subject><subject>Nasopharyngeal Neoplasms - metabolism</subject><subject>Nasopharyngeal Neoplasms - pathology</subject><subject>Proteins - genetics</subject><subject>Proteins - metabolism</subject><subject>Science</subject><subject>Throat cancer</subject><subject>Transforming Growth Factor beta1 - metabolism</subject><subject>Transforming growth factor-b1</subject><subject>Tumors</subject><subject>Vimentin</subject><subject>Vimentin - metabolism</subject><issn>2045-2322</issn><issn>2045-2322</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>C6C</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>eNplkc9qFTEUxoMottQufAEJuFFhNP8n40KQ4m2Fq27qOmQyZ-6kzCRjMiN27xP5ID6TKbdeq4ZADpwf3_lOPoQeU_KSEq5f5QSzYJLU99AxI0JWjDN2_059hE5zviLlSNYI2jxER0zTRnNdH6PvF3434M2Hj1uO4ducIGcfA55TnOICGQeb4zzYdB12YEfsbHI-xMliB-OIJ1hsLtfn1zjFEbAP-PJ8U_38QSsfutVBh2H2ywCjt9USqwkyBDdcT0VrSTZkv5Rxj9CD3o4ZTm_fE_R58-7y7KLafjp_f_Z2WzlJxFIJrljd1h3TABKkFLzuQQnXU6GccNaJvqVt09W1ktxp2zLX2r51DYNW9bTjJ-jNXnde2wk6B6F4GM2c_FQ2NNF683cn-MHs4lcjOWm0kEXg2a1Ail9WyIuZfL75CRsgrtlQrbRqmOCkoE__Qa_imkJZzzAlSgBS8aZQz_eUSzGXJPuDGUrMTbzmEG9hn9x1fyB_h1mAF3sgl1bJK_0Z-b_aL86RsxQ</recordid><startdate>20170215</startdate><enddate>20170215</enddate><creator>Wu, Yanxia</creator><creator>Shen, Zhihua</creator><creator>Wang, Keke</creator><creator>Ha, Yanping</creator><creator>Lei, Hong</creator><creator>Jia, Yanan</creator><creator>Ding, Ranran</creator><creator>Wu, Dongmei</creator><creator>Gan, Siyuan</creator><creator>Li, Rujia</creator><creator>Luo, Botao</creator><creator>Jiang, Hanguo</creator><creator>Jie, Wei</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</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>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20170215</creationdate><title>High FMNL3 expression promotes nasopharyngeal carcinoma cell metastasis: role in TGF-β1-induced epithelia-to-mesenchymal transition</title><author>Wu, Yanxia ; Shen, Zhihua ; Wang, Keke ; Ha, Yanping ; Lei, Hong ; Jia, Yanan ; Ding, Ranran ; Wu, Dongmei ; Gan, Siyuan ; Li, Rujia ; Luo, Botao ; Jiang, Hanguo ; Jie, Wei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c504t-43627b7d28ee5e55437fe64cf146c4cac4fb1b9d77653c8ab2cbafbc92eb6f1d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>13/109</topic><topic>13/89</topic><topic>14/19</topic><topic>38/77</topic><topic>64/60</topic><topic>692/4028/67/322</topic><topic>692/420/755</topic><topic>82</topic><topic>82/80</topic><topic>Adult</topic><topic>Aged</topic><topic>Biomarkers</topic><topic>Cadherins - metabolism</topic><topic>Carcinoma - genetics</topic><topic>Carcinoma - metabolism</topic><topic>Carcinoma - pathology</topic><topic>Cell adhesion & migration</topic><topic>Cell differentiation</topic><topic>Cell Line, Tumor</topic><topic>Cell migration</topic><topic>Cell Movement</topic><topic>Cytoskeleton</topic><topic>E-cadherin</topic><topic>Epithelial-Mesenchymal Transition - drug effects</topic><topic>Epithelial-Mesenchymal Transition - genetics</topic><topic>Female</topic><topic>Formins</topic><topic>Gene Expression</topic><topic>Humanities and Social Sciences</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Lymph nodes</topic><topic>Male</topic><topic>Mesenchyme</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>Middle Aged</topic><topic>multidisciplinary</topic><topic>Nasopharyngeal Carcinoma</topic><topic>Nasopharyngeal Neoplasms - genetics</topic><topic>Nasopharyngeal Neoplasms - metabolism</topic><topic>Nasopharyngeal Neoplasms - pathology</topic><topic>Proteins - genetics</topic><topic>Proteins - metabolism</topic><topic>Science</topic><topic>Throat cancer</topic><topic>Transforming Growth Factor beta1 - metabolism</topic><topic>Transforming growth factor-b1</topic><topic>Tumors</topic><topic>Vimentin</topic><topic>Vimentin - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wu, Yanxia</creatorcontrib><creatorcontrib>Shen, Zhihua</creatorcontrib><creatorcontrib>Wang, Keke</creatorcontrib><creatorcontrib>Ha, Yanping</creatorcontrib><creatorcontrib>Lei, Hong</creatorcontrib><creatorcontrib>Jia, Yanan</creatorcontrib><creatorcontrib>Ding, Ranran</creatorcontrib><creatorcontrib>Wu, Dongmei</creatorcontrib><creatorcontrib>Gan, Siyuan</creatorcontrib><creatorcontrib>Li, Rujia</creatorcontrib><creatorcontrib>Luo, Botao</creatorcontrib><creatorcontrib>Jiang, Hanguo</creatorcontrib><creatorcontrib>Jie, Wei</creatorcontrib><collection>Springer Nature OA/Free 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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest SciTech 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>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>Proquest Central</collection><collection>Natural Science Collection</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 Central Student</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>Science Database</collection><collection>Biological Science Database</collection><collection>Access via ProQuest (Open Access)</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 Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Scientific reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wu, Yanxia</au><au>Shen, Zhihua</au><au>Wang, Keke</au><au>Ha, Yanping</au><au>Lei, Hong</au><au>Jia, Yanan</au><au>Ding, Ranran</au><au>Wu, Dongmei</au><au>Gan, Siyuan</au><au>Li, Rujia</au><au>Luo, Botao</au><au>Jiang, Hanguo</au><au>Jie, Wei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>High FMNL3 expression promotes nasopharyngeal carcinoma cell metastasis: role in TGF-β1-induced epithelia-to-mesenchymal transition</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2017-02-15</date><risdate>2017</risdate><volume>7</volume><issue>1</issue><spage>42507</spage><epage>42507</epage><pages>42507-42507</pages><artnum>42507</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>Formin-like 3 (FMNL3) plays a crucial role in cytoskeletal mediation and is potentially a biomarker for cell migration; however, its role in cancer metastasis remains unknown. In this study, we found elevated FMNL3 protein expression in clinical nasopharyngeal carcinoma (NPC) tissues. FMNL3 expression positively correlated to the clinical stage, T (tumour), N (lymph node metastasis) and M (distant metastasis) classification of NPC patients. Moreover, FMNL3 positively correlated to Vimentin expression and negatively correlated to E-cadherin expression in clinical NPC samples.
In vitro
experiments showed that FMNL3 expression was inversely related to NPC cell differentiation status. Overexpression of FMNL3 led to epithelial-to-mesenchymal transition (EMT) in well differentiated CNE1 cells. TGF-β1-treated poorly differentiated CNE2 cells showed changes in EMT accompanied by enhanced FMNL3 expression and cell migration. On the contrary, knockdown of FMNL3 partially attenuated the TGF-β1-promoted CNE2 cell migration, together with associated changes in EMT markers. Finally, knockdown of FMNL3 also weakened EMT in tumours in xenographs. Our study indicates for the first time that TGF-β1/FMNL3 signalling may be a novel mechanism mediating EMT in NPC, which is closely associated with NPC metastasis.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>28198387</pmid><doi>10.1038/srep42507</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 13/109 13/89 14/19 38/77 64/60 692/4028/67/322 692/420/755 82 82/80 Adult Aged Biomarkers Cadherins - metabolism Carcinoma - genetics Carcinoma - metabolism Carcinoma - pathology Cell adhesion & migration Cell differentiation Cell Line, Tumor Cell migration Cell Movement Cytoskeleton E-cadherin Epithelial-Mesenchymal Transition - drug effects Epithelial-Mesenchymal Transition - genetics Female Formins Gene Expression Humanities and Social Sciences Humans Immunohistochemistry Lymph nodes Male Mesenchyme Metastases Metastasis Middle Aged multidisciplinary Nasopharyngeal Carcinoma Nasopharyngeal Neoplasms - genetics Nasopharyngeal Neoplasms - metabolism Nasopharyngeal Neoplasms - pathology Proteins - genetics Proteins - metabolism Science Throat cancer Transforming Growth Factor beta1 - metabolism Transforming growth factor-b1 Tumors Vimentin Vimentin - metabolism |
| title | High FMNL3 expression promotes nasopharyngeal carcinoma cell metastasis: role in TGF-β1-induced epithelia-to-mesenchymal transition |
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