WNT-1 inducible signaling pathway protein-1 enhances growth and tumorigenesis in human breast cancer
WNT1 inducible signaling pathway protein 1 (WISP1) plays a key role in many cellular functions in a highly tissue-specific manner; however the role of WISP1 in breast cancer is still poorly understood. Here, we demonstrate that WISP1 acts as an oncogene in human breast cancer. We demonstrated that h...
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| Veröffentlicht in: | Scientific reports 2015-03, Vol.5 (1), p.8686-8686, Article 8686 |
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| creator | Chiang, Kun-Chun Yeh, Chun-Nan Chung, Li-Chuan Feng, Tsui-Hsia Sun, Chi-Chin Chen, Miin-Fu Jan, Yi-Yin Yeh, Ta-Sen Chen, Shin-Cheh Juang, Horng-Heng |
| description | WNT1 inducible signaling pathway protein 1 (WISP1) plays a key role in many cellular functions in a highly tissue-specific manner; however the role of WISP1 in breast cancer is still poorly understood. Here, we demonstrate that WISP1 acts as an oncogene in human breast cancer. We demonstrated that human breast cancer tissues had higher WISP1 mRNA expression than normal breast tissues and that treatment of recombinant WISP1 enhanced breast cancer cell proliferation. Further, ectopic expression of WISP1 increased the growth of breast cancer cells
in vitro
and
in vivo
. WISP1 transfection also induced epithelial-mesenchymal-transition (EMT) in MCF-7 cells, leading to higher migration and invasion. During this EMT-inducing process, E-cadherin was repressed and N-cadherin, snail and β-catenin were upregulated. Filamentous actin (F-actin) remodeling and polarization were also observed after WISP1 transfection into MCF-7 cells. Moreover, forced overexpression of WISP1 blocked the expression of NDRG1, a breast cancer tumor suppressor gene. Our study provides novel evidence that WISP1-modulated NDRG1 gene expression is dependent on a DNA fragment (−128 to +46) located within the human NDRG1 promoter. Thus, we concluded that WISP1 is a human breast cancer oncogene and is a potential therapeutic target. |
| doi_str_mv | 10.1038/srep08686 |
| format | Article |
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in vitro
and
in vivo
. WISP1 transfection also induced epithelial-mesenchymal-transition (EMT) in MCF-7 cells, leading to higher migration and invasion. During this EMT-inducing process, E-cadherin was repressed and N-cadherin, snail and β-catenin were upregulated. Filamentous actin (F-actin) remodeling and polarization were also observed after WISP1 transfection into MCF-7 cells. Moreover, forced overexpression of WISP1 blocked the expression of NDRG1, a breast cancer tumor suppressor gene. Our study provides novel evidence that WISP1-modulated NDRG1 gene expression is dependent on a DNA fragment (−128 to +46) located within the human NDRG1 promoter. Thus, we concluded that WISP1 is a human breast cancer oncogene and is a potential therapeutic target.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/srep08686</identifier><identifier>PMID: 25732125</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>14 ; 14/35 ; 631/67/1347 ; 631/80 ; 82 ; 82/1 ; Actin ; Actins - biosynthesis ; Breast cancer ; Breast Neoplasms - genetics ; Breast Neoplasms - pathology ; CCN Intercellular Signaling Proteins - genetics ; Cell Cycle - genetics ; Cell Cycle Proteins - genetics ; Cell Line, Tumor ; Cell Movement - genetics ; Cell Proliferation ; Cell Transformation, Neoplastic - genetics ; Deoxyribonucleic acid ; DNA ; E-cadherin ; Ectopic expression ; Female ; Gene Expression ; Gene Knockdown Techniques ; Humanities and Social Sciences ; Humans ; Intracellular Signaling Peptides and Proteins - genetics ; MCF-7 Cells ; Mesenchyme ; multidisciplinary ; N-Cadherin ; NDRG1 gene ; Oncogenes ; Polarization ; Proto-Oncogene Proteins - genetics ; Science ; Signal transduction ; Transfection ; Tumor suppressor genes ; Tumorigenesis ; Wnt protein ; Wnt1 Protein - genetics ; Wnt1 Protein - metabolism ; β-Catenin</subject><ispartof>Scientific reports, 2015-03, Vol.5 (1), p.8686-8686, Article 8686</ispartof><rights>The Author(s) 2015</rights><rights>Copyright Nature Publishing Group Mar 2015</rights><rights>Copyright © 2015, Macmillan Publishers Limited. All rights reserved 2015 Macmillan Publishers Limited. All rights reserved</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c438t-8b6941ee83d21173c6d32d37ff2bb38ef2d39c9f9827c0f4318b3da0fecbe7333</citedby><cites>FETCH-LOGICAL-c438t-8b6941ee83d21173c6d32d37ff2bb38ef2d39c9f9827c0f4318b3da0fecbe7333</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/PMC4346832/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4346832/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27903,27904,41099,42168,51554,53769,53771</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25732125$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chiang, Kun-Chun</creatorcontrib><creatorcontrib>Yeh, Chun-Nan</creatorcontrib><creatorcontrib>Chung, Li-Chuan</creatorcontrib><creatorcontrib>Feng, Tsui-Hsia</creatorcontrib><creatorcontrib>Sun, Chi-Chin</creatorcontrib><creatorcontrib>Chen, Miin-Fu</creatorcontrib><creatorcontrib>Jan, Yi-Yin</creatorcontrib><creatorcontrib>Yeh, Ta-Sen</creatorcontrib><creatorcontrib>Chen, Shin-Cheh</creatorcontrib><creatorcontrib>Juang, Horng-Heng</creatorcontrib><title>WNT-1 inducible signaling pathway protein-1 enhances growth and tumorigenesis in human breast cancer</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>WNT1 inducible signaling pathway protein 1 (WISP1) plays a key role in many cellular functions in a highly tissue-specific manner; however the role of WISP1 in breast cancer is still poorly understood. Here, we demonstrate that WISP1 acts as an oncogene in human breast cancer. We demonstrated that human breast cancer tissues had higher WISP1 mRNA expression than normal breast tissues and that treatment of recombinant WISP1 enhanced breast cancer cell proliferation. Further, ectopic expression of WISP1 increased the growth of breast cancer cells
in vitro
and
in vivo
. WISP1 transfection also induced epithelial-mesenchymal-transition (EMT) in MCF-7 cells, leading to higher migration and invasion. During this EMT-inducing process, E-cadherin was repressed and N-cadherin, snail and β-catenin were upregulated. Filamentous actin (F-actin) remodeling and polarization were also observed after WISP1 transfection into MCF-7 cells. Moreover, forced overexpression of WISP1 blocked the expression of NDRG1, a breast cancer tumor suppressor gene. Our study provides novel evidence that WISP1-modulated NDRG1 gene expression is dependent on a DNA fragment (−128 to +46) located within the human NDRG1 promoter. Thus, we concluded that WISP1 is a human breast cancer oncogene and is a potential therapeutic target.</description><subject>14</subject><subject>14/35</subject><subject>631/67/1347</subject><subject>631/80</subject><subject>82</subject><subject>82/1</subject><subject>Actin</subject><subject>Actins - biosynthesis</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - pathology</subject><subject>CCN Intercellular Signaling Proteins - genetics</subject><subject>Cell Cycle - genetics</subject><subject>Cell Cycle Proteins - genetics</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement - genetics</subject><subject>Cell Proliferation</subject><subject>Cell Transformation, Neoplastic - genetics</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>E-cadherin</subject><subject>Ectopic expression</subject><subject>Female</subject><subject>Gene Expression</subject><subject>Gene Knockdown Techniques</subject><subject>Humanities and Social Sciences</subject><subject>Humans</subject><subject>Intracellular Signaling Peptides and Proteins - genetics</subject><subject>MCF-7 Cells</subject><subject>Mesenchyme</subject><subject>multidisciplinary</subject><subject>N-Cadherin</subject><subject>NDRG1 gene</subject><subject>Oncogenes</subject><subject>Polarization</subject><subject>Proto-Oncogene Proteins - genetics</subject><subject>Science</subject><subject>Signal transduction</subject><subject>Transfection</subject><subject>Tumor suppressor genes</subject><subject>Tumorigenesis</subject><subject>Wnt protein</subject><subject>Wnt1 Protein - genetics</subject><subject>Wnt1 Protein - metabolism</subject><subject>β-Catenin</subject><issn>2045-2322</issn><issn>2045-2322</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</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>eNplkdFr1TAUxoMobsw9-A9IwBcdVJOcNk1fhDF0CkNfJj6GND1tM9qkJq1j_7253Hm56nnJOZwf3_nIR8hLzt5xBup9irgwJZV8Qk4FK6tCgBBPj_oTcp7SHctViabkzXNyIqoaBBfVKel-fL0tOHW-26xrJ6TJDd5Mzg90Met4bx7oEsOKzmcK_Wi8xUSHGO7XkRrf0XWbQ3QDekwuZR06brPxtI1o0krtjo8vyLPeTAnPH98z8v3Tx9urz8XNt-svV5c3hS1BrYVqZfaHqKATnNdgZQeig7rvRduCwj4PjW36Ronasr4ErlroDOvRtlgDwBn5sNddtnbGzqJfo5n0Et1s4oMOxum_N96Negi_dAmlVCCywJtHgRh-bphWPbtkcZqMx7AlzaVksuJ1vbv1-h_0Lmwxf12mVKOkaECoTL3dUzaGlJPqD2Y407v49CG-zL46dn8g_4SVgYs9kPLKDxiPTv6n9hvWl6Vm</recordid><startdate>20150303</startdate><enddate>20150303</enddate><creator>Chiang, Kun-Chun</creator><creator>Yeh, Chun-Nan</creator><creator>Chung, Li-Chuan</creator><creator>Feng, Tsui-Hsia</creator><creator>Sun, Chi-Chin</creator><creator>Chen, Miin-Fu</creator><creator>Jan, Yi-Yin</creator><creator>Yeh, Ta-Sen</creator><creator>Chen, Shin-Cheh</creator><creator>Juang, Horng-Heng</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>AEUYN</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>20150303</creationdate><title>WNT-1 inducible signaling pathway protein-1 enhances growth and tumorigenesis in human breast cancer</title><author>Chiang, Kun-Chun ; Yeh, Chun-Nan ; Chung, Li-Chuan ; Feng, Tsui-Hsia ; Sun, Chi-Chin ; Chen, Miin-Fu ; Jan, Yi-Yin ; Yeh, Ta-Sen ; Chen, Shin-Cheh ; Juang, Horng-Heng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c438t-8b6941ee83d21173c6d32d37ff2bb38ef2d39c9f9827c0f4318b3da0fecbe7333</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>14</topic><topic>14/35</topic><topic>631/67/1347</topic><topic>631/80</topic><topic>82</topic><topic>82/1</topic><topic>Actin</topic><topic>Actins - biosynthesis</topic><topic>Breast cancer</topic><topic>Breast Neoplasms - genetics</topic><topic>Breast Neoplasms - pathology</topic><topic>CCN Intercellular Signaling Proteins - genetics</topic><topic>Cell Cycle - genetics</topic><topic>Cell Cycle Proteins - genetics</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement - genetics</topic><topic>Cell Proliferation</topic><topic>Cell Transformation, Neoplastic - genetics</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>E-cadherin</topic><topic>Ectopic expression</topic><topic>Female</topic><topic>Gene Expression</topic><topic>Gene Knockdown Techniques</topic><topic>Humanities and Social Sciences</topic><topic>Humans</topic><topic>Intracellular Signaling Peptides and Proteins - genetics</topic><topic>MCF-7 Cells</topic><topic>Mesenchyme</topic><topic>multidisciplinary</topic><topic>N-Cadherin</topic><topic>NDRG1 gene</topic><topic>Oncogenes</topic><topic>Polarization</topic><topic>Proto-Oncogene Proteins - genetics</topic><topic>Science</topic><topic>Signal transduction</topic><topic>Transfection</topic><topic>Tumor suppressor genes</topic><topic>Tumorigenesis</topic><topic>Wnt protein</topic><topic>Wnt1 Protein - genetics</topic><topic>Wnt1 Protein - metabolism</topic><topic>β-Catenin</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chiang, Kun-Chun</creatorcontrib><creatorcontrib>Yeh, Chun-Nan</creatorcontrib><creatorcontrib>Chung, Li-Chuan</creatorcontrib><creatorcontrib>Feng, Tsui-Hsia</creatorcontrib><creatorcontrib>Sun, Chi-Chin</creatorcontrib><creatorcontrib>Chen, Miin-Fu</creatorcontrib><creatorcontrib>Jan, Yi-Yin</creatorcontrib><creatorcontrib>Yeh, Ta-Sen</creatorcontrib><creatorcontrib>Chen, Shin-Cheh</creatorcontrib><creatorcontrib>Juang, Horng-Heng</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 One Sustainability</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>Publicly Available Content 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 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>Chiang, Kun-Chun</au><au>Yeh, Chun-Nan</au><au>Chung, Li-Chuan</au><au>Feng, Tsui-Hsia</au><au>Sun, Chi-Chin</au><au>Chen, Miin-Fu</au><au>Jan, Yi-Yin</au><au>Yeh, Ta-Sen</au><au>Chen, Shin-Cheh</au><au>Juang, Horng-Heng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>WNT-1 inducible signaling pathway protein-1 enhances growth and tumorigenesis in human breast cancer</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2015-03-03</date><risdate>2015</risdate><volume>5</volume><issue>1</issue><spage>8686</spage><epage>8686</epage><pages>8686-8686</pages><artnum>8686</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>WNT1 inducible signaling pathway protein 1 (WISP1) plays a key role in many cellular functions in a highly tissue-specific manner; however the role of WISP1 in breast cancer is still poorly understood. Here, we demonstrate that WISP1 acts as an oncogene in human breast cancer. We demonstrated that human breast cancer tissues had higher WISP1 mRNA expression than normal breast tissues and that treatment of recombinant WISP1 enhanced breast cancer cell proliferation. Further, ectopic expression of WISP1 increased the growth of breast cancer cells
in vitro
and
in vivo
. WISP1 transfection also induced epithelial-mesenchymal-transition (EMT) in MCF-7 cells, leading to higher migration and invasion. During this EMT-inducing process, E-cadherin was repressed and N-cadherin, snail and β-catenin were upregulated. Filamentous actin (F-actin) remodeling and polarization were also observed after WISP1 transfection into MCF-7 cells. Moreover, forced overexpression of WISP1 blocked the expression of NDRG1, a breast cancer tumor suppressor gene. Our study provides novel evidence that WISP1-modulated NDRG1 gene expression is dependent on a DNA fragment (−128 to +46) located within the human NDRG1 promoter. Thus, we concluded that WISP1 is a human breast cancer oncogene and is a potential therapeutic target.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>25732125</pmid><doi>10.1038/srep08686</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 14 14/35 631/67/1347 631/80 82 82/1 Actin Actins - biosynthesis Breast cancer Breast Neoplasms - genetics Breast Neoplasms - pathology CCN Intercellular Signaling Proteins - genetics Cell Cycle - genetics Cell Cycle Proteins - genetics Cell Line, Tumor Cell Movement - genetics Cell Proliferation Cell Transformation, Neoplastic - genetics Deoxyribonucleic acid DNA E-cadherin Ectopic expression Female Gene Expression Gene Knockdown Techniques Humanities and Social Sciences Humans Intracellular Signaling Peptides and Proteins - genetics MCF-7 Cells Mesenchyme multidisciplinary N-Cadherin NDRG1 gene Oncogenes Polarization Proto-Oncogene Proteins - genetics Science Signal transduction Transfection Tumor suppressor genes Tumorigenesis Wnt protein Wnt1 Protein - genetics Wnt1 Protein - metabolism β-Catenin |
| title | WNT-1 inducible signaling pathway protein-1 enhances growth and tumorigenesis in human breast cancer |
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