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Suppression of malignancy by Smad3 in mouse embryonic stem cell formed teratoma
Disease associated gene deficient embryonic stem cells can serve as valuable in vitro models to study disease mechanisms and screen drugs. Smad3 mediated TGF-β/Activin/Nodal signaling plays important roles in many biological processes. Despite numerous studies regarding Smad3 function, the role of S...
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| Published in: | Stem cell reviews and reports 2013-10, Vol.9 (5), p.709 |
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| container_issue | 5 |
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| container_title | Stem cell reviews and reports |
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| creator | Li, Peng Chen, Ying Meng, Xiaoming Xiaoming, Meng Kwok, Ka Yin Huang, Xiaoru Choy, Kwong Wai Wang, Chi Chiu Lan, Huiyao Yuan, Ping |
| description | Disease associated gene deficient embryonic stem cells can serve as valuable in vitro models to study disease mechanisms and screen drugs. Smad3 mediated TGF-β/Activin/Nodal signaling plays important roles in many biological processes. Despite numerous studies regarding Smad3 function, the role of Smad3 in mouse ES cells is not well studied. To understand the function of Smad3 in mouse ES cells, we derived Smad3-/- ES cells and wild type ES cells. Smad3-/- ES cells display no defect on self-renewal. They express similar level of pluripotent genes and lineage genes compared to wild type ES cells. However, Smad3 ablation results in transient difference in germ layer marker expression during embryoid body formation. Mesoderm lineage marker expression is significantly reduced in the embryoid body formed by Smad3-/- ES cells compared to wild type ES cells. Intriguingly, subcutaneous injection of Smad3-/- ES cells into nude mice leads to formation of malignant immature teratomas, whilst wild type ES cells tend to form mature teratomas. Smad3-/- ES cell formed teratomas can therefore provide a new model for the study of the mechanism of malignant teratomas. |
| doi_str_mv | 10.1007/s12015-013-9452-5 |
| format | article |
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Smad3 mediated TGF-β/Activin/Nodal signaling plays important roles in many biological processes. Despite numerous studies regarding Smad3 function, the role of Smad3 in mouse ES cells is not well studied. To understand the function of Smad3 in mouse ES cells, we derived Smad3-/- ES cells and wild type ES cells. Smad3-/- ES cells display no defect on self-renewal. They express similar level of pluripotent genes and lineage genes compared to wild type ES cells. However, Smad3 ablation results in transient difference in germ layer marker expression during embryoid body formation. Mesoderm lineage marker expression is significantly reduced in the embryoid body formed by Smad3-/- ES cells compared to wild type ES cells. Intriguingly, subcutaneous injection of Smad3-/- ES cells into nude mice leads to formation of malignant immature teratomas, whilst wild type ES cells tend to form mature teratomas. Smad3-/- ES cell formed teratomas can therefore provide a new model for the study of the mechanism of malignant teratomas.</description><identifier>ISSN: 2629-3269</identifier><identifier>EISSN: 2629-3277</identifier><identifier>DOI: 10.1007/s12015-013-9452-5</identifier><identifier>PMID: 23794057</identifier><language>eng</language><publisher>United States: Springer Nature B.V</publisher><subject>Alkaline Phosphatase - metabolism ; Animals ; Apoptosis - genetics ; Cell Differentiation - genetics ; Cells, Cultured ; Embryoid Bodies - metabolism ; Embryoid Bodies - pathology ; Embryonic Stem Cells - cytology ; Embryonic Stem Cells - metabolism ; Female ; Gene Expression Regulation, Developmental ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Nude ; Pluripotent Stem Cells - cytology ; Pluripotent Stem Cells - metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Smad3 Protein - deficiency ; Smad3 Protein - genetics ; Stem Cell Transplantation - methods ; Teratoma - genetics ; Teratoma - metabolism ; Teratoma - pathology ; Transplantation, Homologous ; Tumor Suppressor Proteins - deficiency ; Tumor Suppressor Proteins - genetics</subject><ispartof>Stem cell reviews and reports, 2013-10, Vol.9 (5), p.709</ispartof><rights>Springer Science+Business Media New York 2013</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c471t-2163b8424d2e842747a4a62eedc5ba204036997f60b0b5ec50f39c63246f7ac43</citedby></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/23794057$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Peng</creatorcontrib><creatorcontrib>Chen, Ying</creatorcontrib><creatorcontrib>Meng, Xiaoming</creatorcontrib><creatorcontrib>Xiaoming, Meng</creatorcontrib><creatorcontrib>Kwok, Ka Yin</creatorcontrib><creatorcontrib>Huang, Xiaoru</creatorcontrib><creatorcontrib>Choy, Kwong Wai</creatorcontrib><creatorcontrib>Wang, Chi Chiu</creatorcontrib><creatorcontrib>Lan, Huiyao</creatorcontrib><creatorcontrib>Yuan, Ping</creatorcontrib><title>Suppression of malignancy by Smad3 in mouse embryonic stem cell formed teratoma</title><title>Stem cell reviews and reports</title><addtitle>Stem Cell Rev Rep</addtitle><description>Disease associated gene deficient embryonic stem cells can serve as valuable in vitro models to study disease mechanisms and screen drugs. Smad3 mediated TGF-β/Activin/Nodal signaling plays important roles in many biological processes. Despite numerous studies regarding Smad3 function, the role of Smad3 in mouse ES cells is not well studied. To understand the function of Smad3 in mouse ES cells, we derived Smad3-/- ES cells and wild type ES cells. Smad3-/- ES cells display no defect on self-renewal. They express similar level of pluripotent genes and lineage genes compared to wild type ES cells. However, Smad3 ablation results in transient difference in germ layer marker expression during embryoid body formation. Mesoderm lineage marker expression is significantly reduced in the embryoid body formed by Smad3-/- ES cells compared to wild type ES cells. Intriguingly, subcutaneous injection of Smad3-/- ES cells into nude mice leads to formation of malignant immature teratomas, whilst wild type ES cells tend to form mature teratomas. Smad3-/- ES cell formed teratomas can therefore provide a new model for the study of the mechanism of malignant teratomas.</description><subject>Alkaline Phosphatase - metabolism</subject><subject>Animals</subject><subject>Apoptosis - genetics</subject><subject>Cell Differentiation - genetics</subject><subject>Cells, Cultured</subject><subject>Embryoid Bodies - metabolism</subject><subject>Embryoid Bodies - pathology</subject><subject>Embryonic Stem Cells - cytology</subject><subject>Embryonic Stem Cells - metabolism</subject><subject>Female</subject><subject>Gene Expression Regulation, Developmental</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Mice, Nude</subject><subject>Pluripotent Stem Cells - cytology</subject><subject>Pluripotent Stem Cells - metabolism</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>Smad3 Protein - deficiency</subject><subject>Smad3 Protein - genetics</subject><subject>Stem Cell Transplantation - methods</subject><subject>Teratoma - genetics</subject><subject>Teratoma - metabolism</subject><subject>Teratoma - pathology</subject><subject>Transplantation, Homologous</subject><subject>Tumor Suppressor Proteins - deficiency</subject><subject>Tumor Suppressor Proteins - genetics</subject><issn>2629-3269</issn><issn>2629-3277</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><recordid>eNo9T01LwzAYDqK4MfcDvEjAczQfb5LlKMMvGOwwPZckTaWjaWbSHvrvLTg9Pc_h-UToltEHRql-LIxTJgllghiQnMgLtOSKGyK41pf_XJkFWpdypJRyQWG2XKMFF9oAlXqJ9ofxdMqhlDb1ODU42q796m3vJ-wmfIi2FrjtcUxjCThEl6fUtx6XIUTsQ9fhJuUYajyEbIcU7Q26amxXwvqMK_T58vyxfSO7_ev79mlHPGg2EM6UcBvgUPMwgwZtwSoeQu2ls3zeKZQxulHUUSeDl7QRxivBQTXaehArdP-be8rpewxlqI5pzP1cWTEQmsEGjJhVd2fV6OaV1Sm30eap-vsvfgBdQFyA</recordid><startdate>20131001</startdate><enddate>20131001</enddate><creator>Li, Peng</creator><creator>Chen, Ying</creator><creator>Meng, Xiaoming</creator><creator>Xiaoming, Meng</creator><creator>Kwok, Ka Yin</creator><creator>Huang, Xiaoru</creator><creator>Choy, Kwong Wai</creator><creator>Wang, Chi Chiu</creator><creator>Lan, Huiyao</creator><creator>Yuan, Ping</creator><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>3V.</scope><scope>7T5</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</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>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope></search><sort><creationdate>20131001</creationdate><title>Suppression of malignancy by Smad3 in mouse embryonic stem cell formed teratoma</title><author>Li, Peng ; Chen, Ying ; Meng, Xiaoming ; Xiaoming, Meng ; Kwok, Ka Yin ; Huang, Xiaoru ; Choy, Kwong Wai ; Wang, Chi Chiu ; Lan, Huiyao ; Yuan, Ping</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c471t-2163b8424d2e842747a4a62eedc5ba204036997f60b0b5ec50f39c63246f7ac43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Alkaline Phosphatase - metabolism</topic><topic>Animals</topic><topic>Apoptosis - genetics</topic><topic>Cell Differentiation - genetics</topic><topic>Cells, Cultured</topic><topic>Embryoid Bodies - metabolism</topic><topic>Embryoid Bodies - pathology</topic><topic>Embryonic Stem Cells - cytology</topic><topic>Embryonic Stem Cells - metabolism</topic><topic>Female</topic><topic>Gene Expression Regulation, Developmental</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Mice, Nude</topic><topic>Pluripotent Stem Cells - cytology</topic><topic>Pluripotent Stem Cells - metabolism</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>Smad3 Protein - deficiency</topic><topic>Smad3 Protein - genetics</topic><topic>Stem Cell Transplantation - methods</topic><topic>Teratoma - genetics</topic><topic>Teratoma - metabolism</topic><topic>Teratoma - pathology</topic><topic>Transplantation, Homologous</topic><topic>Tumor Suppressor Proteins - deficiency</topic><topic>Tumor Suppressor Proteins - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Peng</creatorcontrib><creatorcontrib>Chen, Ying</creatorcontrib><creatorcontrib>Meng, Xiaoming</creatorcontrib><creatorcontrib>Xiaoming, Meng</creatorcontrib><creatorcontrib>Kwok, Ka Yin</creatorcontrib><creatorcontrib>Huang, Xiaoru</creatorcontrib><creatorcontrib>Choy, Kwong Wai</creatorcontrib><creatorcontrib>Wang, Chi Chiu</creatorcontrib><creatorcontrib>Lan, Huiyao</creatorcontrib><creatorcontrib>Yuan, Ping</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</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>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>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</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>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>ProQuest Biological Science Journals</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 China</collection><collection>Genetics Abstracts</collection><jtitle>Stem cell reviews and reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Peng</au><au>Chen, Ying</au><au>Meng, Xiaoming</au><au>Xiaoming, Meng</au><au>Kwok, Ka Yin</au><au>Huang, Xiaoru</au><au>Choy, Kwong Wai</au><au>Wang, Chi Chiu</au><au>Lan, Huiyao</au><au>Yuan, Ping</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Suppression of malignancy by Smad3 in mouse embryonic stem cell formed teratoma</atitle><jtitle>Stem cell reviews and reports</jtitle><addtitle>Stem Cell Rev Rep</addtitle><date>2013-10-01</date><risdate>2013</risdate><volume>9</volume><issue>5</issue><spage>709</spage><pages>709-</pages><issn>2629-3269</issn><eissn>2629-3277</eissn><abstract>Disease associated gene deficient embryonic stem cells can serve as valuable in vitro models to study disease mechanisms and screen drugs. Smad3 mediated TGF-β/Activin/Nodal signaling plays important roles in many biological processes. Despite numerous studies regarding Smad3 function, the role of Smad3 in mouse ES cells is not well studied. To understand the function of Smad3 in mouse ES cells, we derived Smad3-/- ES cells and wild type ES cells. Smad3-/- ES cells display no defect on self-renewal. They express similar level of pluripotent genes and lineage genes compared to wild type ES cells. However, Smad3 ablation results in transient difference in germ layer marker expression during embryoid body formation. Mesoderm lineage marker expression is significantly reduced in the embryoid body formed by Smad3-/- ES cells compared to wild type ES cells. Intriguingly, subcutaneous injection of Smad3-/- ES cells into nude mice leads to formation of malignant immature teratomas, whilst wild type ES cells tend to form mature teratomas. Smad3-/- ES cell formed teratomas can therefore provide a new model for the study of the mechanism of malignant teratomas.</abstract><cop>United States</cop><pub>Springer Nature B.V</pub><pmid>23794057</pmid><doi>10.1007/s12015-013-9452-5</doi></addata></record> |
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| subjects | Alkaline Phosphatase - metabolism Animals Apoptosis - genetics Cell Differentiation - genetics Cells, Cultured Embryoid Bodies - metabolism Embryoid Bodies - pathology Embryonic Stem Cells - cytology Embryonic Stem Cells - metabolism Female Gene Expression Regulation, Developmental Male Mice Mice, Inbred C57BL Mice, Knockout Mice, Nude Pluripotent Stem Cells - cytology Pluripotent Stem Cells - metabolism Reverse Transcriptase Polymerase Chain Reaction Smad3 Protein - deficiency Smad3 Protein - genetics Stem Cell Transplantation - methods Teratoma - genetics Teratoma - metabolism Teratoma - pathology Transplantation, Homologous Tumor Suppressor Proteins - deficiency Tumor Suppressor Proteins - genetics |
| title | Suppression of malignancy by Smad3 in mouse embryonic stem cell formed teratoma |
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