CUTL1 induces epithelial-mesenchymal transition in non-small cell lung cancer
The homeobox transcription factor CUTL1 has been associated with cellular proliferation and cell cycle progression, and CUTL1 functions as an oncogene. The aim of the present study was to investigate whether CUTL1 participates in epithelial-mesenchymal transition (EMT). The expression levels of CUTL...
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| Veröffentlicht in: | Oncology reports 2017-05, Vol.37 (5), p.3068-3074 |
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| creator | Wang, Junfeng Wang, Yanbo Sun, Dawei Ren, Fenghai Pang, Sainan Xu, Shidong |
| description | The homeobox transcription factor CUTL1 has been associated with cellular proliferation and cell cycle progression, and CUTL1 functions as an oncogene. The aim of the present study was to investigate whether CUTL1 participates in epithelial-mesenchymal transition (EMT). The expression levels of CUTL1, E-cadherin, N-cadherin and Snail were determined by immunohistochemistry assay, immunofluorescence assay or real-time quantitative reverse transcription PCR. Their roles in non-small cell lung cancer (NSCLC) were assessed by functional analyses. Protein expression was detected by western blot analysis. The CUTL1 expression levels are higher in non-small cell lung cancer (NSCLC) tissues. High CUTL1 expression in NSCLC is associated with the mesenchymal-like phenotype. Mechanistically, CUTL1 upregulates transforming growth factor β receptor I (TβR-I) expression, and the TβR-I inhibitor SB431542 abolishes EMT elicited by ectopic CUTL1 expression. Transforming growth factor β (TGF-β) signaling is essential for CUTL1-induced EMT in NSCLC cells. CUTL1 is downstream of TGF-β signaling and CUTL1 is involved in the expression of the TβR-I. This study indicates that CUTL1 may be a potential target for anti-lung cancer therapy. |
| doi_str_mv | 10.3892/or.2017.5571 |
| format | Article |
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The aim of the present study was to investigate whether CUTL1 participates in epithelial-mesenchymal transition (EMT). The expression levels of CUTL1, E-cadherin, N-cadherin and Snail were determined by immunohistochemistry assay, immunofluorescence assay or real-time quantitative reverse transcription PCR. Their roles in non-small cell lung cancer (NSCLC) were assessed by functional analyses. Protein expression was detected by western blot analysis. The CUTL1 expression levels are higher in non-small cell lung cancer (NSCLC) tissues. High CUTL1 expression in NSCLC is associated with the mesenchymal-like phenotype. Mechanistically, CUTL1 upregulates transforming growth factor β receptor I (TβR-I) expression, and the TβR-I inhibitor SB431542 abolishes EMT elicited by ectopic CUTL1 expression. Transforming growth factor β (TGF-β) signaling is essential for CUTL1-induced EMT in NSCLC cells. CUTL1 is downstream of TGF-β signaling and CUTL1 is involved in the expression of the TβR-I. This study indicates that CUTL1 may be a potential target for anti-lung cancer therapy.</description><identifier>ISSN: 1021-335X</identifier><identifier>EISSN: 1791-2431</identifier><identifier>DOI: 10.3892/or.2017.5571</identifier><identifier>PMID: 28405678</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Cancer therapies ; Carcinoma, Non-Small-Cell Lung - genetics ; Carcinoma, Non-Small-Cell Lung - metabolism ; Cell adhesion & migration ; Cell cycle ; Cell Line, Tumor ; Cell Proliferation ; CUTL1 ; Epithelial-Mesenchymal Transition ; Gene Expression Regulation, Neoplastic ; Homeodomain Proteins - genetics ; Homeodomain Proteins - metabolism ; Humans ; Kinases ; Lung cancer ; Lung Neoplasms - genetics ; Lung Neoplasms - metabolism ; Metastasis ; Mortality ; non-small cell lung cancer ; Nuclear Proteins - genetics ; Nuclear Proteins - metabolism ; Patients ; Repressor Proteins - genetics ; Repressor Proteins - metabolism ; Signal Transduction ; Transcription factors ; Transforming Growth Factor beta - metabolism ; transforming growth factor β ; Up-Regulation</subject><ispartof>Oncology reports, 2017-05, Vol.37 (5), p.3068-3074</ispartof><rights>Copyright © 2017, Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c388t-7fdc5f2d98f2eb4266766c7bc24aaa6d37ec24191790d9512a834274c70ac21e3</citedby><cites>FETCH-LOGICAL-c388t-7fdc5f2d98f2eb4266766c7bc24aaa6d37ec24191790d9512a834274c70ac21e3</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/28405678$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Junfeng</creatorcontrib><creatorcontrib>Wang, Yanbo</creatorcontrib><creatorcontrib>Sun, Dawei</creatorcontrib><creatorcontrib>Ren, Fenghai</creatorcontrib><creatorcontrib>Pang, Sainan</creatorcontrib><creatorcontrib>Xu, Shidong</creatorcontrib><title>CUTL1 induces epithelial-mesenchymal transition in non-small cell lung cancer</title><title>Oncology reports</title><addtitle>Oncol Rep</addtitle><description>The homeobox transcription factor CUTL1 has been associated with cellular proliferation and cell cycle progression, and CUTL1 functions as an oncogene. The aim of the present study was to investigate whether CUTL1 participates in epithelial-mesenchymal transition (EMT). The expression levels of CUTL1, E-cadherin, N-cadherin and Snail were determined by immunohistochemistry assay, immunofluorescence assay or real-time quantitative reverse transcription PCR. Their roles in non-small cell lung cancer (NSCLC) were assessed by functional analyses. Protein expression was detected by western blot analysis. The CUTL1 expression levels are higher in non-small cell lung cancer (NSCLC) tissues. High CUTL1 expression in NSCLC is associated with the mesenchymal-like phenotype. Mechanistically, CUTL1 upregulates transforming growth factor β receptor I (TβR-I) expression, and the TβR-I inhibitor SB431542 abolishes EMT elicited by ectopic CUTL1 expression. Transforming growth factor β (TGF-β) signaling is essential for CUTL1-induced EMT in NSCLC cells. CUTL1 is downstream of TGF-β signaling and CUTL1 is involved in the expression of the TβR-I. This study indicates that CUTL1 may be a potential target for anti-lung cancer therapy.</description><subject>Cancer therapies</subject><subject>Carcinoma, Non-Small-Cell Lung - genetics</subject><subject>Carcinoma, Non-Small-Cell Lung - metabolism</subject><subject>Cell adhesion & migration</subject><subject>Cell cycle</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation</subject><subject>CUTL1</subject><subject>Epithelial-Mesenchymal Transition</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Homeodomain Proteins - genetics</subject><subject>Homeodomain Proteins - metabolism</subject><subject>Humans</subject><subject>Kinases</subject><subject>Lung cancer</subject><subject>Lung Neoplasms - genetics</subject><subject>Lung Neoplasms - metabolism</subject><subject>Metastasis</subject><subject>Mortality</subject><subject>non-small cell lung cancer</subject><subject>Nuclear Proteins - genetics</subject><subject>Nuclear Proteins - metabolism</subject><subject>Patients</subject><subject>Repressor Proteins - genetics</subject><subject>Repressor Proteins - metabolism</subject><subject>Signal Transduction</subject><subject>Transcription factors</subject><subject>Transforming Growth Factor beta - metabolism</subject><subject>transforming growth factor β</subject><subject>Up-Regulation</subject><issn>1021-335X</issn><issn>1791-2431</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNpd0E1LAzEQBuAgitaPm2dZEMSDqckku0mOUvyCihcFbyHNZnXLblKT3YP_3pTWHrwkw_AwzLwInVMyZVLBbYhTIFRMy1LQPTShQlEMnNH9XBOgmLHy4wgdp7QkBASp1CE6AslJWQk5QS-z97c5LVpfj9alwq3a4ct1relw75Lz9uunN10xRONTO7TBZ1n44HHK7a6wLj_d6D8La7x18RQdNKZL7mz7n6D3h_u32ROevz4-z-7m2DIpByya2pYN1Eo24BYcqkpUlRULC9wYU9VMuFxSlW8htSopGMk4CG4FMRaoYyfoejN3FcP36NKg-zatlzHehTFpKqXgAPnETC__0WUYo8_baao4BUW5gqxuNsrGkFJ0jV7FtjfxR1Oi1zHrEPU6Zr2OOfOL7dBx0bt6h_9yzeBqA9LK-LqtQ9qZEDETmJSYkUqyX37hg4c</recordid><startdate>20170501</startdate><enddate>20170501</enddate><creator>Wang, Junfeng</creator><creator>Wang, Yanbo</creator><creator>Sun, Dawei</creator><creator>Ren, Fenghai</creator><creator>Pang, Sainan</creator><creator>Xu, Shidong</creator><general>D.A. Spandidos</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>20170501</creationdate><title>CUTL1 induces epithelial-mesenchymal transition in non-small cell lung cancer</title><author>Wang, Junfeng ; Wang, Yanbo ; Sun, Dawei ; Ren, Fenghai ; Pang, Sainan ; Xu, Shidong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c388t-7fdc5f2d98f2eb4266766c7bc24aaa6d37ec24191790d9512a834274c70ac21e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Cancer therapies</topic><topic>Carcinoma, Non-Small-Cell Lung - genetics</topic><topic>Carcinoma, Non-Small-Cell Lung - metabolism</topic><topic>Cell adhesion & migration</topic><topic>Cell cycle</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation</topic><topic>CUTL1</topic><topic>Epithelial-Mesenchymal Transition</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Homeodomain Proteins - genetics</topic><topic>Homeodomain Proteins - metabolism</topic><topic>Humans</topic><topic>Kinases</topic><topic>Lung cancer</topic><topic>Lung Neoplasms - genetics</topic><topic>Lung Neoplasms - metabolism</topic><topic>Metastasis</topic><topic>Mortality</topic><topic>non-small cell lung cancer</topic><topic>Nuclear Proteins - genetics</topic><topic>Nuclear Proteins - metabolism</topic><topic>Patients</topic><topic>Repressor Proteins - genetics</topic><topic>Repressor Proteins - metabolism</topic><topic>Signal Transduction</topic><topic>Transcription factors</topic><topic>Transforming Growth Factor beta - metabolism</topic><topic>transforming growth factor β</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Junfeng</creatorcontrib><creatorcontrib>Wang, Yanbo</creatorcontrib><creatorcontrib>Sun, Dawei</creatorcontrib><creatorcontrib>Ren, Fenghai</creatorcontrib><creatorcontrib>Pang, Sainan</creatorcontrib><creatorcontrib>Xu, Shidong</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>Wang, Junfeng</au><au>Wang, Yanbo</au><au>Sun, Dawei</au><au>Ren, Fenghai</au><au>Pang, Sainan</au><au>Xu, Shidong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CUTL1 induces epithelial-mesenchymal transition in non-small cell lung cancer</atitle><jtitle>Oncology reports</jtitle><addtitle>Oncol Rep</addtitle><date>2017-05-01</date><risdate>2017</risdate><volume>37</volume><issue>5</issue><spage>3068</spage><epage>3074</epage><pages>3068-3074</pages><issn>1021-335X</issn><eissn>1791-2431</eissn><abstract>The homeobox transcription factor CUTL1 has been associated with cellular proliferation and cell cycle progression, and CUTL1 functions as an oncogene. The aim of the present study was to investigate whether CUTL1 participates in epithelial-mesenchymal transition (EMT). The expression levels of CUTL1, E-cadherin, N-cadherin and Snail were determined by immunohistochemistry assay, immunofluorescence assay or real-time quantitative reverse transcription PCR. Their roles in non-small cell lung cancer (NSCLC) were assessed by functional analyses. Protein expression was detected by western blot analysis. The CUTL1 expression levels are higher in non-small cell lung cancer (NSCLC) tissues. High CUTL1 expression in NSCLC is associated with the mesenchymal-like phenotype. Mechanistically, CUTL1 upregulates transforming growth factor β receptor I (TβR-I) expression, and the TβR-I inhibitor SB431542 abolishes EMT elicited by ectopic CUTL1 expression. Transforming growth factor β (TGF-β) signaling is essential for CUTL1-induced EMT in NSCLC cells. CUTL1 is downstream of TGF-β signaling and CUTL1 is involved in the expression of the TβR-I. This study indicates that CUTL1 may be a potential target for anti-lung cancer therapy.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>28405678</pmid><doi>10.3892/or.2017.5571</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Cancer therapies Carcinoma, Non-Small-Cell Lung - genetics Carcinoma, Non-Small-Cell Lung - metabolism Cell adhesion & migration Cell cycle Cell Line, Tumor Cell Proliferation CUTL1 Epithelial-Mesenchymal Transition Gene Expression Regulation, Neoplastic Homeodomain Proteins - genetics Homeodomain Proteins - metabolism Humans Kinases Lung cancer Lung Neoplasms - genetics Lung Neoplasms - metabolism Metastasis Mortality non-small cell lung cancer Nuclear Proteins - genetics Nuclear Proteins - metabolism Patients Repressor Proteins - genetics Repressor Proteins - metabolism Signal Transduction Transcription factors Transforming Growth Factor beta - metabolism transforming growth factor β Up-Regulation |
| title | CUTL1 induces epithelial-mesenchymal transition in non-small cell lung cancer |
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