Oncogenic suppression of PHLPP1 in human melanoma
Akt is constitutively activated in up to 70% of human melanomas and has an important role in the pathogenesis of the disease. However, little is known about protein phosphatases that dephosphorylate and thereby inactivate it in melanoma cells. Here we report that suppression of pleckstrin homology d...
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| Veröffentlicht in: | Oncogene 2014-09, Vol.33 (39), p.4756-4766 |
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| creator | Dong, L Jin, L Tseng, H-Y Wang, C Y Wilmott, J S Yosufi, B Yan, X G Jiang, C C Scolyer, R A Zhang, X D Guo, S T |
| description | Akt is constitutively activated in up to 70% of human melanomas and has an important role in the pathogenesis of the disease. However, little is known about protein phosphatases that dephosphorylate and thereby inactivate it in melanoma cells. Here we report that suppression of pleckstrin homology domain and leucine-rich repeat Ser/Thr protein phosphatase 1 (PHLPP1) by DNA methylation promotes Akt activation and has an oncogenic role in melanoma. While it is commonly downregulated, overexpression of PHLPP1 reduces Akt activation and inhibits melanoma cell proliferation
in vitro
, and retards melanoma growth in a xenograft model. In contrast, knockdown of PHLPP1 increases Akt activation, enhances melanoma cell and melanocyte proliferation, and results in anchorage-independent growth of melanocytes. Suppression of PHLPP1 involves blockade of binding of the transcription factor Sp1 to the
PHLPP1
promoter. Collectively, these results suggest that suppression of PHLPP1 by DNA methylation contributes to melanoma development and progression. |
| doi_str_mv | 10.1038/onc.2013.420 |
| format | Article |
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in vitro
, and retards melanoma growth in a xenograft model. In contrast, knockdown of PHLPP1 increases Akt activation, enhances melanoma cell and melanocyte proliferation, and results in anchorage-independent growth of melanocytes. Suppression of PHLPP1 involves blockade of binding of the transcription factor Sp1 to the
PHLPP1
promoter. Collectively, these results suggest that suppression of PHLPP1 by DNA methylation contributes to melanoma development and progression.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/onc.2013.420</identifier><identifier>PMID: 24121273</identifier><identifier>CODEN: ONCNES</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>631/337/176/1988 ; 631/80/86 ; 692/699/67/1813/1634 ; AKT protein ; Animals ; Apoptosis ; Cell activation ; Cell Biology ; Cell Line, Tumor ; Cell Proliferation ; Cell Survival ; Development and progression ; DNA Methylation ; Down-Regulation ; Enzyme Activation ; Gene Expression Regulation, Neoplastic ; Gene Silencing ; Genetic aspects ; Homology ; Human Genetics ; Humans ; Internal Medicine ; Male ; Medicine ; Medicine & Public Health ; Melanocytes ; Melanoma ; Melanoma - genetics ; Melanoma - metabolism ; Melanoma - pathology ; Mice ; Mice, Nude ; Nuclear Proteins - genetics ; Nuclear Proteins - metabolism ; Oncology ; original-article ; Pathogenesis ; Phosphatases ; Phosphatidylinositol 3-Kinases - metabolism ; Phosphoprotein phosphatase ; Phosphoprotein Phosphatases - genetics ; Phosphoprotein Phosphatases - metabolism ; Pleckstrin ; Promoter Regions, Genetic ; Properties ; Protein phosphatase ; Proto-Oncogene Proteins c-akt - metabolism ; Sp1 protein ; Sp1 Transcription Factor - metabolism ; Tumor Burden ; Xenografts</subject><ispartof>Oncogene, 2014-09, Vol.33 (39), p.4756-4766</ispartof><rights>Macmillan Publishers Limited 2014</rights><rights>COPYRIGHT 2014 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Sep 25, 2014</rights><rights>Macmillan Publishers Limited 2014.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c593t-78f521ca5a2dbf52ed965e1f645f1761ad7b905696032196ed91d1d124c807a03</citedby><cites>FETCH-LOGICAL-c593t-78f521ca5a2dbf52ed965e1f645f1761ad7b905696032196ed91d1d124c807a03</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.2013.420$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/onc.2013.420$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24121273$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Dong, L</creatorcontrib><creatorcontrib>Jin, L</creatorcontrib><creatorcontrib>Tseng, H-Y</creatorcontrib><creatorcontrib>Wang, C Y</creatorcontrib><creatorcontrib>Wilmott, J S</creatorcontrib><creatorcontrib>Yosufi, B</creatorcontrib><creatorcontrib>Yan, X G</creatorcontrib><creatorcontrib>Jiang, C C</creatorcontrib><creatorcontrib>Scolyer, R A</creatorcontrib><creatorcontrib>Zhang, X D</creatorcontrib><creatorcontrib>Guo, S T</creatorcontrib><title>Oncogenic suppression of PHLPP1 in human melanoma</title><title>Oncogene</title><addtitle>Oncogene</addtitle><addtitle>Oncogene</addtitle><description>Akt is constitutively activated in up to 70% of human melanomas and has an important role in the pathogenesis of the disease. However, little is known about protein phosphatases that dephosphorylate and thereby inactivate it in melanoma cells. Here we report that suppression of pleckstrin homology domain and leucine-rich repeat Ser/Thr protein phosphatase 1 (PHLPP1) by DNA methylation promotes Akt activation and has an oncogenic role in melanoma. While it is commonly downregulated, overexpression of PHLPP1 reduces Akt activation and inhibits melanoma cell proliferation
in vitro
, and retards melanoma growth in a xenograft model. In contrast, knockdown of PHLPP1 increases Akt activation, enhances melanoma cell and melanocyte proliferation, and results in anchorage-independent growth of melanocytes. Suppression of PHLPP1 involves blockade of binding of the transcription factor Sp1 to the
PHLPP1
promoter. Collectively, these results suggest that suppression of PHLPP1 by DNA methylation contributes to melanoma development and progression.</description><subject>631/337/176/1988</subject><subject>631/80/86</subject><subject>692/699/67/1813/1634</subject><subject>AKT protein</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Cell activation</subject><subject>Cell Biology</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation</subject><subject>Cell Survival</subject><subject>Development and progression</subject><subject>DNA Methylation</subject><subject>Down-Regulation</subject><subject>Enzyme Activation</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Gene Silencing</subject><subject>Genetic aspects</subject><subject>Homology</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Melanocytes</subject><subject>Melanoma</subject><subject>Melanoma - genetics</subject><subject>Melanoma - metabolism</subject><subject>Melanoma - pathology</subject><subject>Mice</subject><subject>Mice, Nude</subject><subject>Nuclear Proteins - genetics</subject><subject>Nuclear Proteins - metabolism</subject><subject>Oncology</subject><subject>original-article</subject><subject>Pathogenesis</subject><subject>Phosphatases</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Phosphoprotein phosphatase</subject><subject>Phosphoprotein Phosphatases - genetics</subject><subject>Phosphoprotein Phosphatases - metabolism</subject><subject>Pleckstrin</subject><subject>Promoter Regions, Genetic</subject><subject>Properties</subject><subject>Protein phosphatase</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Sp1 protein</subject><subject>Sp1 Transcription Factor - metabolism</subject><subject>Tumor Burden</subject><subject>Xenografts</subject><issn>0950-9232</issn><issn>1476-5594</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqFkc1PGzEQxa2KqqS0N85oJS49sOnM-GPXR4QoVIpEDu3ZcrzesChrBzt74L_HUeinUKs52PL85nmeHmOnCHME3n6Owc0JkM8FwRs2Q9GoWkotjtgMtIRaE6dj9j7nBwBoNNA7dkwCCanhM4Z3wcW1D4Or8rTdJp_zEEMV-2p5u1gusRpCdT-NNlSj39gQR_uBve3tJvuPL-cJ-_7l-tvVbb24u_l6dbmondR8VzdtLwmdlZa6Vbn6TivpsVdC9tgotF2z0iCVVsAJtSp97EqRcC00FvgJ-3TQ3ab4OPm8M-OQnd-ULXycskFFpBDaFv-PSqUQUZMs6Plf6EOcUihGDCmBkqMS8C-qaAmplRLtL2ptN94MoY-7ZN3-a3PJW0nFGe615q9QpTo_Di4G3w_l_Y-Bi8OASzHn5HuzTcNo05NBMPvITYnc7CM3JfKCn73sOq1G3_2Ef2RcgPoA5NIKa59-M_Oa4DPML68E</recordid><startdate>20140925</startdate><enddate>20140925</enddate><creator>Dong, L</creator><creator>Jin, L</creator><creator>Tseng, H-Y</creator><creator>Wang, C Y</creator><creator>Wilmott, J S</creator><creator>Yosufi, B</creator><creator>Yan, X G</creator><creator>Jiang, C C</creator><creator>Scolyer, R A</creator><creator>Zhang, X D</creator><creator>Guo, S T</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</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>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>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20140925</creationdate><title>Oncogenic suppression of PHLPP1 in human melanoma</title><author>Dong, L ; Jin, L ; Tseng, H-Y ; Wang, C Y ; Wilmott, J S ; Yosufi, B ; Yan, X G ; Jiang, C C ; Scolyer, R A ; Zhang, X D ; Guo, S T</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c593t-78f521ca5a2dbf52ed965e1f645f1761ad7b905696032196ed91d1d124c807a03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>631/337/176/1988</topic><topic>631/80/86</topic><topic>692/699/67/1813/1634</topic><topic>AKT protein</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Cell activation</topic><topic>Cell Biology</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation</topic><topic>Cell Survival</topic><topic>Development and progression</topic><topic>DNA Methylation</topic><topic>Down-Regulation</topic><topic>Enzyme Activation</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Gene Silencing</topic><topic>Genetic aspects</topic><topic>Homology</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Internal Medicine</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Melanocytes</topic><topic>Melanoma</topic><topic>Melanoma - 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Academic</collection><jtitle>Oncogene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Dong, L</au><au>Jin, L</au><au>Tseng, H-Y</au><au>Wang, C Y</au><au>Wilmott, J S</au><au>Yosufi, B</au><au>Yan, X G</au><au>Jiang, C C</au><au>Scolyer, R A</au><au>Zhang, X D</au><au>Guo, S T</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Oncogenic suppression of PHLPP1 in human melanoma</atitle><jtitle>Oncogene</jtitle><stitle>Oncogene</stitle><addtitle>Oncogene</addtitle><date>2014-09-25</date><risdate>2014</risdate><volume>33</volume><issue>39</issue><spage>4756</spage><epage>4766</epage><pages>4756-4766</pages><issn>0950-9232</issn><eissn>1476-5594</eissn><coden>ONCNES</coden><abstract>Akt is constitutively activated in up to 70% of human melanomas and has an important role in the pathogenesis of the disease. However, little is known about protein phosphatases that dephosphorylate and thereby inactivate it in melanoma cells. Here we report that suppression of pleckstrin homology domain and leucine-rich repeat Ser/Thr protein phosphatase 1 (PHLPP1) by DNA methylation promotes Akt activation and has an oncogenic role in melanoma. While it is commonly downregulated, overexpression of PHLPP1 reduces Akt activation and inhibits melanoma cell proliferation
in vitro
, and retards melanoma growth in a xenograft model. In contrast, knockdown of PHLPP1 increases Akt activation, enhances melanoma cell and melanocyte proliferation, and results in anchorage-independent growth of melanocytes. Suppression of PHLPP1 involves blockade of binding of the transcription factor Sp1 to the
PHLPP1
promoter. Collectively, these results suggest that suppression of PHLPP1 by DNA methylation contributes to melanoma development and progression.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>24121273</pmid><doi>10.1038/onc.2013.420</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 631/337/176/1988 631/80/86 692/699/67/1813/1634 AKT protein Animals Apoptosis Cell activation Cell Biology Cell Line, Tumor Cell Proliferation Cell Survival Development and progression DNA Methylation Down-Regulation Enzyme Activation Gene Expression Regulation, Neoplastic Gene Silencing Genetic aspects Homology Human Genetics Humans Internal Medicine Male Medicine Medicine & Public Health Melanocytes Melanoma Melanoma - genetics Melanoma - metabolism Melanoma - pathology Mice Mice, Nude Nuclear Proteins - genetics Nuclear Proteins - metabolism Oncology original-article Pathogenesis Phosphatases Phosphatidylinositol 3-Kinases - metabolism Phosphoprotein phosphatase Phosphoprotein Phosphatases - genetics Phosphoprotein Phosphatases - metabolism Pleckstrin Promoter Regions, Genetic Properties Protein phosphatase Proto-Oncogene Proteins c-akt - metabolism Sp1 protein Sp1 Transcription Factor - metabolism Tumor Burden Xenografts |
| title | Oncogenic suppression of PHLPP1 in human melanoma |
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