p53 switches off pluripotency on differentiation
The role of p53 as "a guardian of the genome" has been well established in somatic cells. However, its role in pluripotent stem cells remains much more elusive. Here, we discuss research progress in understanding the role of p53 in pluripotent stem cells and in pluripotent stem cell-like c...
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Veröffentlicht in: | Stem cell research & therapy 2017-02, Vol.8 (1), p.44-44, Article 44 |
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description | The role of p53 as "a guardian of the genome" has been well established in somatic cells. However, its role in pluripotent stem cells remains much more elusive. Here, we discuss research progress in understanding the role of p53 in pluripotent stem cells and in pluripotent stem cell-like cancer stem cells. The p53 protein, which plays a key role in embryonic stem cells, was first discovered in 2005. Landmark studies of p53-related reprogramming elucidated this protein's importance in induced pluripotent stem cells in 2009. The p53-related safety concerns in pluripotent stem cells have been raised in stem cell-based therapy although the use of iPSCs in therapeutic application is promising. Because cancer stem cells have profiles similar to those of pluripotent stem cells, we also describe potential strategies for studies in cancer stem cells and cancer treatments. The new discoveries of p53 family proteins in pluripotent stem cells have made possible stable progress in stem cell transplantation efficiency and safety, as well as treatment strategies targeting cancer stem cells based on pluripotent stem cell technology. |
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However, its role in pluripotent stem cells remains much more elusive. Here, we discuss research progress in understanding the role of p53 in pluripotent stem cells and in pluripotent stem cell-like cancer stem cells. The p53 protein, which plays a key role in embryonic stem cells, was first discovered in 2005. Landmark studies of p53-related reprogramming elucidated this protein's importance in induced pluripotent stem cells in 2009. The p53-related safety concerns in pluripotent stem cells have been raised in stem cell-based therapy although the use of iPSCs in therapeutic application is promising. Because cancer stem cells have profiles similar to those of pluripotent stem cells, we also describe potential strategies for studies in cancer stem cells and cancer treatments. The new discoveries of p53 family proteins in pluripotent stem cells have made possible stable progress in stem cell transplantation efficiency and safety, as well as treatment strategies targeting cancer stem cells based on pluripotent stem cell technology.</description><identifier>ISSN: 1757-6512</identifier><identifier>EISSN: 1757-6512</identifier><identifier>DOI: 10.1186/s13287-017-0498-1</identifier><identifier>PMID: 28241890</identifier><language>eng</language><publisher>England: BioMed Central</publisher><subject>Animals ; Cell Differentiation ; Cell- and Tissue-Based Therapy ; Embryonic Stem Cells ; Gene Expression Regulation, Neoplastic ; Humans ; Mice ; Molecular Targeted Therapy ; Neoplasms - genetics ; Neoplasms - metabolism ; Neoplasms - pathology ; Neoplasms - therapy ; Neoplastic Stem Cells ; Pluripotent Stem Cells - cytology ; Pluripotent Stem Cells - metabolism ; Review ; Signal Transduction ; Stem Cell Transplantation ; Tumor Suppressor Protein p53 - genetics ; Tumor Suppressor Protein p53 - metabolism</subject><ispartof>Stem cell research & therapy, 2017-02, Vol.8 (1), p.44-44, Article 44</ispartof><rights>Copyright BioMed Central 2017</rights><rights>The Author(s). 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c526t-6dc46d2af19cf916b0687ed7ee74e81539900719c6a7b06590cfc18ec6d6483f3</citedby><cites>FETCH-LOGICAL-c526t-6dc46d2af19cf916b0687ed7ee74e81539900719c6a7b06590cfc18ec6d6483f3</cites><orcidid>0000-0001-7033-6982</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5330084/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5330084/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28241890$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lin, Tongxiang</creatorcontrib><creatorcontrib>Lin, Yi</creatorcontrib><title>p53 switches off pluripotency on differentiation</title><title>Stem cell research & therapy</title><addtitle>Stem Cell Res Ther</addtitle><description>The role of p53 as "a guardian of the genome" has been well established in somatic cells. However, its role in pluripotent stem cells remains much more elusive. Here, we discuss research progress in understanding the role of p53 in pluripotent stem cells and in pluripotent stem cell-like cancer stem cells. The p53 protein, which plays a key role in embryonic stem cells, was first discovered in 2005. Landmark studies of p53-related reprogramming elucidated this protein's importance in induced pluripotent stem cells in 2009. The p53-related safety concerns in pluripotent stem cells have been raised in stem cell-based therapy although the use of iPSCs in therapeutic application is promising. Because cancer stem cells have profiles similar to those of pluripotent stem cells, we also describe potential strategies for studies in cancer stem cells and cancer treatments. The new discoveries of p53 family proteins in pluripotent stem cells have made possible stable progress in stem cell transplantation efficiency and safety, as well as treatment strategies targeting cancer stem cells based on pluripotent stem cell technology.</description><subject>Animals</subject><subject>Cell Differentiation</subject><subject>Cell- and Tissue-Based Therapy</subject><subject>Embryonic Stem Cells</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Humans</subject><subject>Mice</subject><subject>Molecular Targeted Therapy</subject><subject>Neoplasms - genetics</subject><subject>Neoplasms - metabolism</subject><subject>Neoplasms - pathology</subject><subject>Neoplasms - therapy</subject><subject>Neoplastic Stem Cells</subject><subject>Pluripotent Stem Cells - cytology</subject><subject>Pluripotent Stem Cells - metabolism</subject><subject>Review</subject><subject>Signal Transduction</subject><subject>Stem Cell Transplantation</subject><subject>Tumor Suppressor Protein p53 - genetics</subject><subject>Tumor Suppressor Protein p53 - metabolism</subject><issn>1757-6512</issn><issn>1757-6512</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</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>eNqNUV1LwzAUDaK4MfcDfJGCL75Uc9s0SV8EGX7BwBd9DlmauIyuqUmr7N-bsjmmTwZCAvfcc889B6FzwNcAnN4EyDPOUgzxkpKncITGwAqW0gKy44P_CE1DWOF48hxjSk7RKOMZAV7iMcJtkSfhy3ZqqUPijEnauve2dZ1u1CZxTVJZY7TXTWdlZ11zhk6MrIOe7t4Jenu4f509pfOXx-fZ3TxVRUa7lFaK0CqTBkplSqALTDnTFdOaEc2hyMsSYxaLVLJYK0qsjAKuFa0o4bnJJ-h2y9v2i7WuVBTgZS1ab9fSb4STVvyuNHYp3t2nKIYtOYkEVzsC7z56HTqxtkHpupaNdn0QwDkwmmGg_4CyaDUrorAJuvwDXbneN9GJAUU4jy4Ps2GLUt6F4LXZ6wYshvTENj0R0xNDegJiz8XhwvuOn6zybwLVk-I</recordid><startdate>20170228</startdate><enddate>20170228</enddate><creator>Lin, Tongxiang</creator><creator>Lin, Yi</creator><general>BioMed Central</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>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>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>7QO</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-7033-6982</orcidid></search><sort><creationdate>20170228</creationdate><title>p53 switches off pluripotency on differentiation</title><author>Lin, Tongxiang ; Lin, Yi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c526t-6dc46d2af19cf916b0687ed7ee74e81539900719c6a7b06590cfc18ec6d6483f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Animals</topic><topic>Cell Differentiation</topic><topic>Cell- and Tissue-Based Therapy</topic><topic>Embryonic Stem Cells</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Humans</topic><topic>Mice</topic><topic>Molecular Targeted Therapy</topic><topic>Neoplasms - genetics</topic><topic>Neoplasms - metabolism</topic><topic>Neoplasms - pathology</topic><topic>Neoplasms - therapy</topic><topic>Neoplastic Stem Cells</topic><topic>Pluripotent Stem Cells - cytology</topic><topic>Pluripotent Stem Cells - metabolism</topic><topic>Review</topic><topic>Signal Transduction</topic><topic>Stem Cell Transplantation</topic><topic>Tumor Suppressor Protein p53 - genetics</topic><topic>Tumor Suppressor Protein p53 - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lin, Tongxiang</creatorcontrib><creatorcontrib>Lin, Yi</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 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>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>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 China</collection><collection>MEDLINE - Academic</collection><collection>Biotechnology Research Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Stem cell research & therapy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lin, Tongxiang</au><au>Lin, Yi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>p53 switches off pluripotency on differentiation</atitle><jtitle>Stem cell research & therapy</jtitle><addtitle>Stem Cell Res Ther</addtitle><date>2017-02-28</date><risdate>2017</risdate><volume>8</volume><issue>1</issue><spage>44</spage><epage>44</epage><pages>44-44</pages><artnum>44</artnum><issn>1757-6512</issn><eissn>1757-6512</eissn><abstract>The role of p53 as "a guardian of the genome" has been well established in somatic cells. However, its role in pluripotent stem cells remains much more elusive. Here, we discuss research progress in understanding the role of p53 in pluripotent stem cells and in pluripotent stem cell-like cancer stem cells. The p53 protein, which plays a key role in embryonic stem cells, was first discovered in 2005. Landmark studies of p53-related reprogramming elucidated this protein's importance in induced pluripotent stem cells in 2009. The p53-related safety concerns in pluripotent stem cells have been raised in stem cell-based therapy although the use of iPSCs in therapeutic application is promising. Because cancer stem cells have profiles similar to those of pluripotent stem cells, we also describe potential strategies for studies in cancer stem cells and cancer treatments. 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subjects | Animals Cell Differentiation Cell- and Tissue-Based Therapy Embryonic Stem Cells Gene Expression Regulation, Neoplastic Humans Mice Molecular Targeted Therapy Neoplasms - genetics Neoplasms - metabolism Neoplasms - pathology Neoplasms - therapy Neoplastic Stem Cells Pluripotent Stem Cells - cytology Pluripotent Stem Cells - metabolism Review Signal Transduction Stem Cell Transplantation Tumor Suppressor Protein p53 - genetics Tumor Suppressor Protein p53 - metabolism |
title | p53 switches off pluripotency on differentiation |
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