Forkhead box C1 induces epithelial-mesenchymal transition and is a potential therapeutic target in nasopharyngeal carcinoma
Nasopharyngeal carcinoma (NPC) is a highly invasive malignancy with cervical lymphopathy as the initial presentation. Epithelial-mesenchymal transition (EMT), a process by which epithelial cells lose cell-cell adhesion and gain migratory and invasive properties, has a pivotal role in metastasis. For...
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| Veröffentlicht in: | Molecular medicine reports 2015-12, Vol.12 (6), p.8003-8009 |
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| creator | OU-YANG, LEI XIAO, SHENG-JUN LIU, PENG YI, SHI-JANG ZHANG, XIAO-LING OU-YANG, SHI TAN, SHENG-KUI LEI, XUN |
| description | Nasopharyngeal carcinoma (NPC) is a highly invasive malignancy with cervical lymphopathy as the initial presentation. Epithelial-mesenchymal transition (EMT), a process by which epithelial cells lose cell-cell adhesion and gain migratory and invasive properties, has a pivotal role in metastasis. Forkhead box C1 (FoxC1), a member of the forkhead family of transcription factors, induces EMT and has a critical role in metastasis of multiple human cancers. However, the role of FoxC1 in the progression of NPC has remained elusive. The present study revealed that the expression of FoxC1 was markedly elevated in NPC tissues compared with that in chronically inflamed nasopharyngeal tissues and was closely correlated with vimentin, fibronectin and N-cadherin expression as indicated by immunohisto-chemical assays. In addition, high FoxC1 expression was positively associated with lymph node metastasis, distant metastasis and an advanced clinical stage in patients with NPC. Furthermore, FoxC1 expression was high in NPC cell lines while being low in an immortalized normal nasopharyngeal epithelial cell line. In vitro, knockdown of FoxC1 in the CNE2 human NPC cell line by small interfering RNA downregulated vimentin, fibronectin and N-cadherin expression and reduced the migratory and invasive capacity of CNE2 cells. In conclusion, the present study indicated that FoxC1 has a pivotal role in EMT through the upregulation of vimentin, fibronectin and N-cadherin expression. Thus, FoxC1 may be a potential therapeutic target in NPC. |
| doi_str_mv | 10.3892/mmr.2015.4427 |
| format | Article |
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Epithelial-mesenchymal transition (EMT), a process by which epithelial cells lose cell-cell adhesion and gain migratory and invasive properties, has a pivotal role in metastasis. Forkhead box C1 (FoxC1), a member of the forkhead family of transcription factors, induces EMT and has a critical role in metastasis of multiple human cancers. However, the role of FoxC1 in the progression of NPC has remained elusive. The present study revealed that the expression of FoxC1 was markedly elevated in NPC tissues compared with that in chronically inflamed nasopharyngeal tissues and was closely correlated with vimentin, fibronectin and N-cadherin expression as indicated by immunohisto-chemical assays. In addition, high FoxC1 expression was positively associated with lymph node metastasis, distant metastasis and an advanced clinical stage in patients with NPC. Furthermore, FoxC1 expression was high in NPC cell lines while being low in an immortalized normal nasopharyngeal epithelial cell line. In vitro, knockdown of FoxC1 in the CNE2 human NPC cell line by small interfering RNA downregulated vimentin, fibronectin and N-cadherin expression and reduced the migratory and invasive capacity of CNE2 cells. In conclusion, the present study indicated that FoxC1 has a pivotal role in EMT through the upregulation of vimentin, fibronectin and N-cadherin expression. Thus, FoxC1 may be a potential therapeutic target in NPC.</description><identifier>ISSN: 1791-2997</identifier><identifier>EISSN: 1791-3004</identifier><identifier>DOI: 10.3892/mmr.2015.4427</identifier><identifier>PMID: 26461269</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Adult ; Biotechnology ; Breast cancer ; Cadherins ; Cadherins - metabolism ; Carcinoma ; Care and treatment ; Cell adhesion ; Cell adhesion & migration ; Cell Line, Tumor ; Cell migration ; Cell Movement ; Cervix ; Classification ; Epithelial cells ; Epithelial-Mesenchymal Transition ; epithelial-mesenchymal transition nasopharyngeal carcinoma ; Extracellular matrix ; Female ; Fibronectin ; Fibronectins - metabolism ; forkhead box C1 ; Forkhead protein ; Forkhead Transcription Factors - antagonists & inhibitors ; Forkhead Transcription Factors - genetics ; Forkhead Transcription Factors - metabolism ; Gene Expression Regulation, Neoplastic ; Genes ; Genetic aspects ; Humans ; Immunohistochemistry ; Inflammation ; Invasiveness ; Liver cancer ; Lung cancer ; Lymph nodes ; Lymphatic Metastasis ; Male ; Malignancy ; Mesenchyme ; Metastases ; Metastasis ; Middle Aged ; N-Cadherin ; Nasopharyngeal cancer ; Nasopharyngeal Carcinoma ; Nasopharyngeal Neoplasms - metabolism ; Nasopharyngeal Neoplasms - pathology ; Physiological aspects ; RNA Interference ; RNA, Small Interfering - metabolism ; siRNA ; Studies ; Throat cancer ; Transcription factors ; Vimentin ; Vimentin - metabolism</subject><ispartof>Molecular medicine reports, 2015-12, Vol.12 (6), p.8003-8009</ispartof><rights>Copyright: © Ou-Yang et al.</rights><rights>COPYRIGHT 2015 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2015</rights><rights>Copyright: © Ou-Yang et al. 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c580t-52211a392905ad06f1f46c454b8cc42acf8b29fd648cc7ed82402575a3dc55923</citedby><cites>FETCH-LOGICAL-c580t-52211a392905ad06f1f46c454b8cc42acf8b29fd648cc7ed82402575a3dc55923</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,315,781,785,886,5572,27926,27927</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26461269$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>OU-YANG, LEI</creatorcontrib><creatorcontrib>XIAO, SHENG-JUN</creatorcontrib><creatorcontrib>LIU, PENG</creatorcontrib><creatorcontrib>YI, SHI-JANG</creatorcontrib><creatorcontrib>ZHANG, XIAO-LING</creatorcontrib><creatorcontrib>OU-YANG, SHI</creatorcontrib><creatorcontrib>TAN, SHENG-KUI</creatorcontrib><creatorcontrib>LEI, XUN</creatorcontrib><title>Forkhead box C1 induces epithelial-mesenchymal transition and is a potential therapeutic target in nasopharyngeal carcinoma</title><title>Molecular medicine reports</title><addtitle>Mol Med Rep</addtitle><description>Nasopharyngeal carcinoma (NPC) is a highly invasive malignancy with cervical lymphopathy as the initial presentation. Epithelial-mesenchymal transition (EMT), a process by which epithelial cells lose cell-cell adhesion and gain migratory and invasive properties, has a pivotal role in metastasis. Forkhead box C1 (FoxC1), a member of the forkhead family of transcription factors, induces EMT and has a critical role in metastasis of multiple human cancers. However, the role of FoxC1 in the progression of NPC has remained elusive. The present study revealed that the expression of FoxC1 was markedly elevated in NPC tissues compared with that in chronically inflamed nasopharyngeal tissues and was closely correlated with vimentin, fibronectin and N-cadherin expression as indicated by immunohisto-chemical assays. In addition, high FoxC1 expression was positively associated with lymph node metastasis, distant metastasis and an advanced clinical stage in patients with NPC. Furthermore, FoxC1 expression was high in NPC cell lines while being low in an immortalized normal nasopharyngeal epithelial cell line. In vitro, knockdown of FoxC1 in the CNE2 human NPC cell line by small interfering RNA downregulated vimentin, fibronectin and N-cadherin expression and reduced the migratory and invasive capacity of CNE2 cells. In conclusion, the present study indicated that FoxC1 has a pivotal role in EMT through the upregulation of vimentin, fibronectin and N-cadherin expression. Thus, FoxC1 may be a potential therapeutic target in NPC.</description><subject>Adult</subject><subject>Biotechnology</subject><subject>Breast cancer</subject><subject>Cadherins</subject><subject>Cadherins - metabolism</subject><subject>Carcinoma</subject><subject>Care and treatment</subject><subject>Cell adhesion</subject><subject>Cell adhesion & migration</subject><subject>Cell Line, Tumor</subject><subject>Cell migration</subject><subject>Cell Movement</subject><subject>Cervix</subject><subject>Classification</subject><subject>Epithelial cells</subject><subject>Epithelial-Mesenchymal Transition</subject><subject>epithelial-mesenchymal transition nasopharyngeal carcinoma</subject><subject>Extracellular matrix</subject><subject>Female</subject><subject>Fibronectin</subject><subject>Fibronectins - metabolism</subject><subject>forkhead box C1</subject><subject>Forkhead protein</subject><subject>Forkhead Transcription Factors - antagonists & inhibitors</subject><subject>Forkhead Transcription Factors - genetics</subject><subject>Forkhead Transcription Factors - metabolism</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Inflammation</subject><subject>Invasiveness</subject><subject>Liver cancer</subject><subject>Lung cancer</subject><subject>Lymph nodes</subject><subject>Lymphatic Metastasis</subject><subject>Male</subject><subject>Malignancy</subject><subject>Mesenchyme</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>Middle Aged</subject><subject>N-Cadherin</subject><subject>Nasopharyngeal cancer</subject><subject>Nasopharyngeal Carcinoma</subject><subject>Nasopharyngeal Neoplasms - metabolism</subject><subject>Nasopharyngeal Neoplasms - pathology</subject><subject>Physiological aspects</subject><subject>RNA Interference</subject><subject>RNA, Small Interfering - metabolism</subject><subject>siRNA</subject><subject>Studies</subject><subject>Throat cancer</subject><subject>Transcription factors</subject><subject>Vimentin</subject><subject>Vimentin - metabolism</subject><issn>1791-2997</issn><issn>1791-3004</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><sourceid>GNUQQ</sourceid><recordid>eNptkk1v1DAQhiMEoqVw5IoscYBLFn8nviBVKwpIlbjA2Zp1nI1LYgfbqaj48zjsslCEfPDHPPN6xn6r6jnBG9Yq-maa4oZiIjac0-ZBdU4aRWqGMX94XFOlmrPqSUo3GEtBhXpcnVHJJaFSnVc_rkL8Oljo0C58R1uCnO8WYxOys8uDHR2M9WST9Wa4m2BEOYJPLrvgEfgOuYQAzSFbn90aHWyE2S7ZGZQh7m0ueshDCvMA8c7vbYEMRON8mOBp9aiHMdlnx_mi-nL17vP2Q3396f3H7eV1bUSLcy0oJQSYogoL6LDsSc-l4YLvWmM4BdO3O6r6TvKyb2zXUo6paASwzgihKLuo3h5052U32c6UYiOMeo5uKkXpAE7fj3g36H241bwRLW1UEXh9FIjh22JT1pNLxo4jeBuWpEnDBGO8kAV9-Q96E5boS3uaKEZ5Q4iUf6g9jFY734dyr1lF9SVnimAlf9W9-Q9VRmcnZ4K3vSvn9xLqQ4KJIaVo-1OPBOvVLbq4Ra9u0atbCv_i74c50b_tUYBXByDN5bddF9KJKUo1oTWWdYsxYz8BqyPJAw</recordid><startdate>20151201</startdate><enddate>20151201</enddate><creator>OU-YANG, LEI</creator><creator>XIAO, SHENG-JUN</creator><creator>LIU, PENG</creator><creator>YI, SHI-JANG</creator><creator>ZHANG, XIAO-LING</creator><creator>OU-YANG, SHI</creator><creator>TAN, SHENG-KUI</creator><creator>LEI, XUN</creator><general>D.A. 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metabolism</topic><topic>Carcinoma</topic><topic>Care and treatment</topic><topic>Cell adhesion</topic><topic>Cell adhesion & migration</topic><topic>Cell Line, Tumor</topic><topic>Cell migration</topic><topic>Cell Movement</topic><topic>Cervix</topic><topic>Classification</topic><topic>Epithelial cells</topic><topic>Epithelial-Mesenchymal Transition</topic><topic>epithelial-mesenchymal transition nasopharyngeal carcinoma</topic><topic>Extracellular matrix</topic><topic>Female</topic><topic>Fibronectin</topic><topic>Fibronectins - metabolism</topic><topic>forkhead box C1</topic><topic>Forkhead protein</topic><topic>Forkhead Transcription Factors - antagonists & inhibitors</topic><topic>Forkhead Transcription Factors - genetics</topic><topic>Forkhead Transcription Factors - metabolism</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genes</topic><topic>Genetic aspects</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Inflammation</topic><topic>Invasiveness</topic><topic>Liver cancer</topic><topic>Lung cancer</topic><topic>Lymph nodes</topic><topic>Lymphatic Metastasis</topic><topic>Male</topic><topic>Malignancy</topic><topic>Mesenchyme</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>Middle Aged</topic><topic>N-Cadherin</topic><topic>Nasopharyngeal cancer</topic><topic>Nasopharyngeal Carcinoma</topic><topic>Nasopharyngeal Neoplasms - metabolism</topic><topic>Nasopharyngeal Neoplasms - pathology</topic><topic>Physiological aspects</topic><topic>RNA Interference</topic><topic>RNA, Small Interfering - metabolism</topic><topic>siRNA</topic><topic>Studies</topic><topic>Throat cancer</topic><topic>Transcription factors</topic><topic>Vimentin</topic><topic>Vimentin - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>OU-YANG, LEI</creatorcontrib><creatorcontrib>XIAO, SHENG-JUN</creatorcontrib><creatorcontrib>LIU, PENG</creatorcontrib><creatorcontrib>YI, SHI-JANG</creatorcontrib><creatorcontrib>ZHANG, XIAO-LING</creatorcontrib><creatorcontrib>OU-YANG, SHI</creatorcontrib><creatorcontrib>TAN, SHENG-KUI</creatorcontrib><creatorcontrib>LEI, XUN</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>ProQuest Pharma Collection</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>British Nursing Database</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>Biological Science 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>Molecular medicine reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>OU-YANG, LEI</au><au>XIAO, SHENG-JUN</au><au>LIU, PENG</au><au>YI, SHI-JANG</au><au>ZHANG, XIAO-LING</au><au>OU-YANG, SHI</au><au>TAN, SHENG-KUI</au><au>LEI, XUN</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Forkhead box C1 induces epithelial-mesenchymal transition and is a potential therapeutic target in nasopharyngeal carcinoma</atitle><jtitle>Molecular medicine reports</jtitle><addtitle>Mol Med Rep</addtitle><date>2015-12-01</date><risdate>2015</risdate><volume>12</volume><issue>6</issue><spage>8003</spage><epage>8009</epage><pages>8003-8009</pages><issn>1791-2997</issn><eissn>1791-3004</eissn><abstract>Nasopharyngeal carcinoma (NPC) is a highly invasive malignancy with cervical lymphopathy as the initial presentation. Epithelial-mesenchymal transition (EMT), a process by which epithelial cells lose cell-cell adhesion and gain migratory and invasive properties, has a pivotal role in metastasis. Forkhead box C1 (FoxC1), a member of the forkhead family of transcription factors, induces EMT and has a critical role in metastasis of multiple human cancers. However, the role of FoxC1 in the progression of NPC has remained elusive. The present study revealed that the expression of FoxC1 was markedly elevated in NPC tissues compared with that in chronically inflamed nasopharyngeal tissues and was closely correlated with vimentin, fibronectin and N-cadherin expression as indicated by immunohisto-chemical assays. In addition, high FoxC1 expression was positively associated with lymph node metastasis, distant metastasis and an advanced clinical stage in patients with NPC. Furthermore, FoxC1 expression was high in NPC cell lines while being low in an immortalized normal nasopharyngeal epithelial cell line. In vitro, knockdown of FoxC1 in the CNE2 human NPC cell line by small interfering RNA downregulated vimentin, fibronectin and N-cadherin expression and reduced the migratory and invasive capacity of CNE2 cells. In conclusion, the present study indicated that FoxC1 has a pivotal role in EMT through the upregulation of vimentin, fibronectin and N-cadherin expression. Thus, FoxC1 may be a potential therapeutic target in NPC.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>26461269</pmid><doi>10.3892/mmr.2015.4427</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Molecular medicine reports, 2015-12, Vol.12 (6), p.8003-8009 |
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| source | Spandidos Publications Journals; MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Adult Biotechnology Breast cancer Cadherins Cadherins - metabolism Carcinoma Care and treatment Cell adhesion Cell adhesion & migration Cell Line, Tumor Cell migration Cell Movement Cervix Classification Epithelial cells Epithelial-Mesenchymal Transition epithelial-mesenchymal transition nasopharyngeal carcinoma Extracellular matrix Female Fibronectin Fibronectins - metabolism forkhead box C1 Forkhead protein Forkhead Transcription Factors - antagonists & inhibitors Forkhead Transcription Factors - genetics Forkhead Transcription Factors - metabolism Gene Expression Regulation, Neoplastic Genes Genetic aspects Humans Immunohistochemistry Inflammation Invasiveness Liver cancer Lung cancer Lymph nodes Lymphatic Metastasis Male Malignancy Mesenchyme Metastases Metastasis Middle Aged N-Cadherin Nasopharyngeal cancer Nasopharyngeal Carcinoma Nasopharyngeal Neoplasms - metabolism Nasopharyngeal Neoplasms - pathology Physiological aspects RNA Interference RNA, Small Interfering - metabolism siRNA Studies Throat cancer Transcription factors Vimentin Vimentin - metabolism |
| title | Forkhead box C1 induces epithelial-mesenchymal transition and is a potential therapeutic target in nasopharyngeal carcinoma |
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