NKX6.1 functions as a metastatic suppressor through epigenetic regulation of the epithelial–mesenchymal transition
The transcription factor NKX6.1 (NK6 homeobox 1) is important in the development of pancreatic β-cells and neurons. Although recent publications show that NKX6.1 is hypermethylated and downregulated during tumorigenesis, the function of NKX6.1 in carcinogenesis remains elusive. Here, we address the...
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| Veröffentlicht in: | Oncogene 2016-04, Vol.35 (17), p.2266-2278 |
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| creator | Li, H-J Yu, P-N Huang, K-Y Su, H-Y Hsiao, T-H Chang, C-P Yu, M-H Lin, Y-W |
| description | The transcription factor NKX6.1 (NK6 homeobox 1) is important in the development of pancreatic β-cells and neurons. Although recent publications show that
NKX6.1
is hypermethylated and downregulated during tumorigenesis, the function of NKX6.1 in carcinogenesis remains elusive. Here, we address the metastasis suppressor function of human NKX6.1 using cell, animal and clinical analyses. Our data show that NKX6.1 represses tumor formation and metastatic ability both
in vitro
and
in vivo
. Mechanistically, NKX6.1 suppresses cell invasion by inhibiting the epithelial-to-mesenchymal transition (EMT). NKX6.1 directly enhances the mRNA level of E-cadherin by recruiting BAF155 coactivator and represses that of vimentin and N-cadherin by recruiting RBBP7 (retinoblastoma binding protein 7) corepressor. Clinical cancer tumors with metastasis show low NKX6.1 protein expression coinciding with low E-cadherin and high vimentin expression. Our results demonstrate that NKX6.1 functions as an EMT suppressor by interacting with different epigenetic modifiers, making it a potential novel therapeutic option. |
| doi_str_mv | 10.1038/onc.2015.289 |
| format | Article |
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NKX6.1
is hypermethylated and downregulated during tumorigenesis, the function of NKX6.1 in carcinogenesis remains elusive. Here, we address the metastasis suppressor function of human NKX6.1 using cell, animal and clinical analyses. Our data show that NKX6.1 represses tumor formation and metastatic ability both
in vitro
and
in vivo
. Mechanistically, NKX6.1 suppresses cell invasion by inhibiting the epithelial-to-mesenchymal transition (EMT). NKX6.1 directly enhances the mRNA level of E-cadherin by recruiting BAF155 coactivator and represses that of vimentin and N-cadherin by recruiting RBBP7 (retinoblastoma binding protein 7) corepressor. Clinical cancer tumors with metastasis show low NKX6.1 protein expression coinciding with low E-cadherin and high vimentin expression. Our results demonstrate that NKX6.1 functions as an EMT suppressor by interacting with different epigenetic modifiers, making it a potential novel therapeutic option.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/onc.2015.289</identifier><identifier>PMID: 26257059</identifier><identifier>CODEN: ONCNES</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/89 ; 38/22 ; 38/70 ; 38/77 ; 38/90 ; 42/109 ; 45 ; 631/67/322 ; 64/60 ; 82 ; 82/51 ; 82/58 ; 82/80 ; 82/83 ; 96/63 ; Animals ; Apoptosis ; Cadherins - biosynthesis ; Cadherins - genetics ; Cancer ; Cell Biology ; Cell Line, Tumor ; DNA Methylation - genetics ; Epigenesis, Genetic ; Epigenetics ; Epithelial-Mesenchymal Transition - drug effects ; Epithelial-Mesenchymal Transition - genetics ; Gene Expression Regulation, Neoplastic - drug effects ; Genes, Tumor Suppressor ; Genetic aspects ; Genetic regulation ; Health aspects ; Homeodomain Proteins - genetics ; Homeodomain Proteins - metabolism ; Human Genetics ; Humans ; Internal Medicine ; Medicine ; Medicine & Public Health ; Metastasis ; Mice ; Neoplasm Invasiveness - genetics ; Oncology ; Original ; original-article ; Prevention ; Properties ; Protein expression ; Retinoblastoma-Binding Protein 7 - genetics ; RNA, Messenger - genetics ; Transcription factors ; Transcription Factors - genetics ; Tumorigenesis ; Vimentin - administration & dosage</subject><ispartof>Oncogene, 2016-04, Vol.35 (17), p.2266-2278</ispartof><rights>The Author(s) 2016</rights><rights>COPYRIGHT 2016 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Apr 28, 2016</rights><rights>Copyright © 2016 Macmillan Publishers Limited 2016 Macmillan Publishers Limited</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c550t-1453c2d128dada2eb9b0e3810249fed5b08f6016da38460872a81d51d668d873</citedby><cites>FETCH-LOGICAL-c550t-1453c2d128dada2eb9b0e3810249fed5b08f6016da38460872a81d51d668d873</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/onc.2015.289$$EPDF$$P50$$Gspringer$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/onc.2015.289$$EHTML$$P50$$Gspringer$$Hfree_for_read</linktohtml><link.rule.ids>230,314,780,784,885,27923,27924,41487,42556,51318</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26257059$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, H-J</creatorcontrib><creatorcontrib>Yu, P-N</creatorcontrib><creatorcontrib>Huang, K-Y</creatorcontrib><creatorcontrib>Su, H-Y</creatorcontrib><creatorcontrib>Hsiao, T-H</creatorcontrib><creatorcontrib>Chang, C-P</creatorcontrib><creatorcontrib>Yu, M-H</creatorcontrib><creatorcontrib>Lin, Y-W</creatorcontrib><title>NKX6.1 functions as a metastatic suppressor through epigenetic regulation of the epithelial–mesenchymal transition</title><title>Oncogene</title><addtitle>Oncogene</addtitle><addtitle>Oncogene</addtitle><description>The transcription factor NKX6.1 (NK6 homeobox 1) is important in the development of pancreatic β-cells and neurons. Although recent publications show that
NKX6.1
is hypermethylated and downregulated during tumorigenesis, the function of NKX6.1 in carcinogenesis remains elusive. Here, we address the metastasis suppressor function of human NKX6.1 using cell, animal and clinical analyses. Our data show that NKX6.1 represses tumor formation and metastatic ability both
in vitro
and
in vivo
. Mechanistically, NKX6.1 suppresses cell invasion by inhibiting the epithelial-to-mesenchymal transition (EMT). NKX6.1 directly enhances the mRNA level of E-cadherin by recruiting BAF155 coactivator and represses that of vimentin and N-cadherin by recruiting RBBP7 (retinoblastoma binding protein 7) corepressor. Clinical cancer tumors with metastasis show low NKX6.1 protein expression coinciding with low E-cadherin and high vimentin expression. Our results demonstrate that NKX6.1 functions as an EMT suppressor by interacting with different epigenetic modifiers, making it a potential novel therapeutic option.</description><subject>13/89</subject><subject>38/22</subject><subject>38/70</subject><subject>38/77</subject><subject>38/90</subject><subject>42/109</subject><subject>45</subject><subject>631/67/322</subject><subject>64/60</subject><subject>82</subject><subject>82/51</subject><subject>82/58</subject><subject>82/80</subject><subject>82/83</subject><subject>96/63</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Cadherins - biosynthesis</subject><subject>Cadherins - genetics</subject><subject>Cancer</subject><subject>Cell Biology</subject><subject>Cell Line, Tumor</subject><subject>DNA Methylation - genetics</subject><subject>Epigenesis, Genetic</subject><subject>Epigenetics</subject><subject>Epithelial-Mesenchymal Transition - drug effects</subject><subject>Epithelial-Mesenchymal Transition - genetics</subject><subject>Gene Expression Regulation, Neoplastic - drug effects</subject><subject>Genes, Tumor Suppressor</subject><subject>Genetic aspects</subject><subject>Genetic regulation</subject><subject>Health aspects</subject><subject>Homeodomain Proteins - genetics</subject><subject>Homeodomain Proteins - metabolism</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Metastasis</subject><subject>Mice</subject><subject>Neoplasm Invasiveness - genetics</subject><subject>Oncology</subject><subject>Original</subject><subject>original-article</subject><subject>Prevention</subject><subject>Properties</subject><subject>Protein expression</subject><subject>Retinoblastoma-Binding Protein 7 - genetics</subject><subject>RNA, Messenger - genetics</subject><subject>Transcription factors</subject><subject>Transcription Factors - genetics</subject><subject>Tumorigenesis</subject><subject>Vimentin - administration & dosage</subject><issn>0950-9232</issn><issn>1476-5594</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNptks9u1DAQxi0EokvhxhlF4sKBLLYTJ_YFqar4Jyq49MDN8tqTrKvEDnZSqTfegTfkSZhoS7VFlS2N5PnNNx77I-Qlo1tGK_kuBrvllIktl-oR2bC6bUohVP2YbKgStFS84ifkWc5XlNJWUf6UnPCGi5YKtSHzt68_mi0ruiXY2ceQC4O7GGE2eTazt0VepilBzjEV8z7Fpd8XMPkeAqzZBP0ymLWyiB0CsCYxDN4Mf379HiFDsPub0QzFnEzIfkWfkyedGTK8uI2n5PLjh8vzz-XF909fzs8uSisEnUtWi8pyx7h0xhkOO7WjUElGea06cGJHZddQ1jhTybqhsuVGMieYaxrpZFudkvcH2WnZjeAsBLzCoKfkR5NudDRe388Ev9d9vNa1xP6tQoE3twIp_lwgz3r02cIwmABxyZq1Ctu0jRKIvv4PvYpLCjgdUrKWDP_liOrNANqHLmJfu4rqMxxWsQZJpLYPULgcjN7GAJ3H83sFbw8FNsWcE3R3MzKqV5NoNIleTaLRJIi_On6XO_ifKxAoD0DGVOghHQ3zkOBfyC_InQ</recordid><startdate>20160428</startdate><enddate>20160428</enddate><creator>Li, H-J</creator><creator>Yu, P-N</creator><creator>Huang, K-Y</creator><creator>Su, H-Y</creator><creator>Hsiao, T-H</creator><creator>Chang, C-P</creator><creator>Yu, M-H</creator><creator>Lin, Y-W</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>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</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>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>RC3</scope><scope>5PM</scope></search><sort><creationdate>20160428</creationdate><title>NKX6.1 functions as a metastatic suppressor through epigenetic regulation of the epithelial–mesenchymal transition</title><author>Li, H-J ; Yu, P-N ; Huang, K-Y ; Su, H-Y ; Hsiao, T-H ; Chang, C-P ; Yu, M-H ; Lin, Y-W</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c550t-1453c2d128dada2eb9b0e3810249fed5b08f6016da38460872a81d51d668d873</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>13/89</topic><topic>38/22</topic><topic>38/70</topic><topic>38/77</topic><topic>38/90</topic><topic>42/109</topic><topic>45</topic><topic>631/67/322</topic><topic>64/60</topic><topic>82</topic><topic>82/51</topic><topic>82/58</topic><topic>82/80</topic><topic>82/83</topic><topic>96/63</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Cadherins - biosynthesis</topic><topic>Cadherins - genetics</topic><topic>Cancer</topic><topic>Cell Biology</topic><topic>Cell Line, Tumor</topic><topic>DNA Methylation - genetics</topic><topic>Epigenesis, Genetic</topic><topic>Epigenetics</topic><topic>Epithelial-Mesenchymal Transition - drug effects</topic><topic>Epithelial-Mesenchymal Transition - genetics</topic><topic>Gene Expression Regulation, Neoplastic - drug effects</topic><topic>Genes, Tumor Suppressor</topic><topic>Genetic aspects</topic><topic>Genetic regulation</topic><topic>Health aspects</topic><topic>Homeodomain Proteins - genetics</topic><topic>Homeodomain Proteins - metabolism</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Internal Medicine</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Metastasis</topic><topic>Mice</topic><topic>Neoplasm Invasiveness - genetics</topic><topic>Oncology</topic><topic>Original</topic><topic>original-article</topic><topic>Prevention</topic><topic>Properties</topic><topic>Protein expression</topic><topic>Retinoblastoma-Binding Protein 7 - genetics</topic><topic>RNA, Messenger - genetics</topic><topic>Transcription factors</topic><topic>Transcription Factors - genetics</topic><topic>Tumorigenesis</topic><topic>Vimentin - administration & dosage</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, H-J</creatorcontrib><creatorcontrib>Yu, P-N</creatorcontrib><creatorcontrib>Huang, K-Y</creatorcontrib><creatorcontrib>Su, H-Y</creatorcontrib><creatorcontrib>Hsiao, T-H</creatorcontrib><creatorcontrib>Chang, C-P</creatorcontrib><creatorcontrib>Yu, M-H</creatorcontrib><creatorcontrib>Lin, Y-W</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>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</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>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</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>Research Library (Alumni Edition)</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>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</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>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Biotechnology and BioEngineering Abstracts</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>Genetics Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oncogene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, H-J</au><au>Yu, P-N</au><au>Huang, K-Y</au><au>Su, H-Y</au><au>Hsiao, T-H</au><au>Chang, C-P</au><au>Yu, M-H</au><au>Lin, Y-W</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>NKX6.1 functions as a metastatic suppressor through epigenetic regulation of the epithelial–mesenchymal transition</atitle><jtitle>Oncogene</jtitle><stitle>Oncogene</stitle><addtitle>Oncogene</addtitle><date>2016-04-28</date><risdate>2016</risdate><volume>35</volume><issue>17</issue><spage>2266</spage><epage>2278</epage><pages>2266-2278</pages><issn>0950-9232</issn><eissn>1476-5594</eissn><coden>ONCNES</coden><abstract>The transcription factor NKX6.1 (NK6 homeobox 1) is important in the development of pancreatic β-cells and neurons. Although recent publications show that
NKX6.1
is hypermethylated and downregulated during tumorigenesis, the function of NKX6.1 in carcinogenesis remains elusive. Here, we address the metastasis suppressor function of human NKX6.1 using cell, animal and clinical analyses. Our data show that NKX6.1 represses tumor formation and metastatic ability both
in vitro
and
in vivo
. Mechanistically, NKX6.1 suppresses cell invasion by inhibiting the epithelial-to-mesenchymal transition (EMT). NKX6.1 directly enhances the mRNA level of E-cadherin by recruiting BAF155 coactivator and represses that of vimentin and N-cadherin by recruiting RBBP7 (retinoblastoma binding protein 7) corepressor. Clinical cancer tumors with metastasis show low NKX6.1 protein expression coinciding with low E-cadherin and high vimentin expression. Our results demonstrate that NKX6.1 functions as an EMT suppressor by interacting with different epigenetic modifiers, making it a potential novel therapeutic option.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>26257059</pmid><doi>10.1038/onc.2015.289</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 13/89 38/22 38/70 38/77 38/90 42/109 45 631/67/322 64/60 82 82/51 82/58 82/80 82/83 96/63 Animals Apoptosis Cadherins - biosynthesis Cadherins - genetics Cancer Cell Biology Cell Line, Tumor DNA Methylation - genetics Epigenesis, Genetic Epigenetics Epithelial-Mesenchymal Transition - drug effects Epithelial-Mesenchymal Transition - genetics Gene Expression Regulation, Neoplastic - drug effects Genes, Tumor Suppressor Genetic aspects Genetic regulation Health aspects Homeodomain Proteins - genetics Homeodomain Proteins - metabolism Human Genetics Humans Internal Medicine Medicine Medicine & Public Health Metastasis Mice Neoplasm Invasiveness - genetics Oncology Original original-article Prevention Properties Protein expression Retinoblastoma-Binding Protein 7 - genetics RNA, Messenger - genetics Transcription factors Transcription Factors - genetics Tumorigenesis Vimentin - administration & dosage |
| title | NKX6.1 functions as a metastatic suppressor through epigenetic regulation of the epithelial–mesenchymal transition |
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