GDF15 promotes EMT and metastasis in colorectal cancer
Metastasis is the major cause of cancer deaths, and the epithelial-mesenchymal transition (EMT) has been considered to be a fundamental event in cancer metastasis. However, the role of growth differentiation factor 15 (GDF15) in colorectal cancer (CRC) metastasis and EMT remains poorly understood. H...
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| Veröffentlicht in: | Oncotarget 2016-01, Vol.7 (1), p.860-872 |
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| creator | Li, Chen Wang, Jingyu Kong, Jianlu Tang, Jinlong Wu, Yihua Xu, Enping Zhang, Honghe Lai, Maode |
| description | Metastasis is the major cause of cancer deaths, and the epithelial-mesenchymal transition (EMT) has been considered to be a fundamental event in cancer metastasis. However, the role of growth differentiation factor 15 (GDF15) in colorectal cancer (CRC) metastasis and EMT remains poorly understood. Here, we showed that GDF15 promoted CRC cell metastasis both in vitro and in vivo. In addition, the EMT process was enhanced by GDF15 through binding to TGF-β receptor to activate Smad2 and Smad3 pathways. Clinical data showed GDF15 level in tumor tissues, and the serum was significantly increased, in which high GDF15 level correlated with a reduced overall survival in CRC. Thus, GDF15 may promote colorectal cancer metastasis through activating EMT. Promisingly, GDF15 could be considered as a novel prognostic marker for CRC in the clinic. |
| doi_str_mv | 10.18632/oncotarget.6205 |
| format | Article |
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However, the role of growth differentiation factor 15 (GDF15) in colorectal cancer (CRC) metastasis and EMT remains poorly understood. Here, we showed that GDF15 promoted CRC cell metastasis both in vitro and in vivo. In addition, the EMT process was enhanced by GDF15 through binding to TGF-β receptor to activate Smad2 and Smad3 pathways. Clinical data showed GDF15 level in tumor tissues, and the serum was significantly increased, in which high GDF15 level correlated with a reduced overall survival in CRC. Thus, GDF15 may promote colorectal cancer metastasis through activating EMT. Promisingly, GDF15 could be considered as a novel prognostic marker for CRC in the clinic.</description><identifier>ISSN: 1949-2553</identifier><identifier>EISSN: 1949-2553</identifier><identifier>DOI: 10.18632/oncotarget.6205</identifier><identifier>PMID: 26497212</identifier><language>eng</language><publisher>United States: Impact Journals LLC</publisher><subject>Animals ; Cell Line, Tumor ; Colorectal Neoplasms - genetics ; Colorectal Neoplasms - metabolism ; Colorectal Neoplasms - pathology ; Epithelial-Mesenchymal Transition - genetics ; Female ; Gene Expression Regulation, Neoplastic ; Growth Differentiation Factor 15 - blood ; Growth Differentiation Factor 15 - genetics ; Growth Differentiation Factor 15 - metabolism ; HEK293 Cells ; HT29 Cells ; Humans ; Immunoblotting ; Immunohistochemistry ; Male ; Mice, Inbred NOD ; Mice, SCID ; Middle Aged ; Neoplasm Metastasis ; Proportional Hazards Models ; Receptors, Transforming Growth Factor beta - genetics ; Receptors, Transforming Growth Factor beta - metabolism ; Research Paper ; Reverse Transcriptase Polymerase Chain Reaction - statistics & numerical data ; RNA Interference ; Smad2 Protein - genetics ; Smad2 Protein - metabolism ; Smad3 Protein - genetics ; Smad3 Protein - metabolism ; Survival Analysis ; Transplantation, Heterologous</subject><ispartof>Oncotarget, 2016-01, Vol.7 (1), p.860-872</ispartof><rights>Copyright: © 2016 Li et al. 2016</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c354t-4f882add07cad5ddf31818a2223c7fb0625eddbac0024939774d5b8ca4c5f97e3</citedby><cites>FETCH-LOGICAL-c354t-4f882add07cad5ddf31818a2223c7fb0625eddbac0024939774d5b8ca4c5f97e3</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/PMC4808038/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4808038/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27903,27904,53769,53771</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26497212$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Chen</creatorcontrib><creatorcontrib>Wang, Jingyu</creatorcontrib><creatorcontrib>Kong, Jianlu</creatorcontrib><creatorcontrib>Tang, Jinlong</creatorcontrib><creatorcontrib>Wu, Yihua</creatorcontrib><creatorcontrib>Xu, Enping</creatorcontrib><creatorcontrib>Zhang, Honghe</creatorcontrib><creatorcontrib>Lai, Maode</creatorcontrib><title>GDF15 promotes EMT and metastasis in colorectal cancer</title><title>Oncotarget</title><addtitle>Oncotarget</addtitle><description>Metastasis is the major cause of cancer deaths, and the epithelial-mesenchymal transition (EMT) has been considered to be a fundamental event in cancer metastasis. However, the role of growth differentiation factor 15 (GDF15) in colorectal cancer (CRC) metastasis and EMT remains poorly understood. Here, we showed that GDF15 promoted CRC cell metastasis both in vitro and in vivo. In addition, the EMT process was enhanced by GDF15 through binding to TGF-β receptor to activate Smad2 and Smad3 pathways. Clinical data showed GDF15 level in tumor tissues, and the serum was significantly increased, in which high GDF15 level correlated with a reduced overall survival in CRC. Thus, GDF15 may promote colorectal cancer metastasis through activating EMT. Promisingly, GDF15 could be considered as a novel prognostic marker for CRC in the clinic.</description><subject>Animals</subject><subject>Cell Line, Tumor</subject><subject>Colorectal Neoplasms - genetics</subject><subject>Colorectal Neoplasms - metabolism</subject><subject>Colorectal Neoplasms - pathology</subject><subject>Epithelial-Mesenchymal Transition - genetics</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Growth Differentiation Factor 15 - blood</subject><subject>Growth Differentiation Factor 15 - genetics</subject><subject>Growth Differentiation Factor 15 - metabolism</subject><subject>HEK293 Cells</subject><subject>HT29 Cells</subject><subject>Humans</subject><subject>Immunoblotting</subject><subject>Immunohistochemistry</subject><subject>Male</subject><subject>Mice, Inbred NOD</subject><subject>Mice, SCID</subject><subject>Middle Aged</subject><subject>Neoplasm Metastasis</subject><subject>Proportional Hazards Models</subject><subject>Receptors, Transforming Growth Factor beta - genetics</subject><subject>Receptors, Transforming Growth Factor beta - metabolism</subject><subject>Research Paper</subject><subject>Reverse Transcriptase Polymerase Chain Reaction - statistics & numerical data</subject><subject>RNA Interference</subject><subject>Smad2 Protein - genetics</subject><subject>Smad2 Protein - metabolism</subject><subject>Smad3 Protein - genetics</subject><subject>Smad3 Protein - metabolism</subject><subject>Survival Analysis</subject><subject>Transplantation, Heterologous</subject><issn>1949-2553</issn><issn>1949-2553</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkE1Lw0AQhhdRbKm9e5IcvaTu98dFkNpWoeKlnpfN7qZGkmzdTQX_vdHWWoeBGZh33hkeAC4RnCDJCb4JrQ2diWvfTTiG7AQMkaIqx4yR06N-AMYpvcE-GBUSq3MwwJwqgREeAr64nyOWbWJoQudTNntaZaZ1WeM7k_qsUla1mQ11iN52ps6saa2PF-CsNHXy430dgZf5bDV9yJfPi8fp3TK3hNEup6WU2DgHhTWOOVcSJJE0GGNiRVlAjpl3rjAWQkwVUUJQxwppDbWsVMKTEbjd-W62ReOd9W0XTa03sWpM_NTBVPr_pK1e9Tp8aCqhhET2Btd7gxjetz51uqmS9XVtWh-2SSPBseKSQ9FL4U5qY0gp-vJwBkH9Q1z_EdffxPuVq-P3Dgu_fMkXu2F_TQ</recordid><startdate>20160105</startdate><enddate>20160105</enddate><creator>Li, Chen</creator><creator>Wang, Jingyu</creator><creator>Kong, Jianlu</creator><creator>Tang, Jinlong</creator><creator>Wu, Yihua</creator><creator>Xu, Enping</creator><creator>Zhang, Honghe</creator><creator>Lai, Maode</creator><general>Impact Journals LLC</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>7X8</scope><scope>5PM</scope></search><sort><creationdate>20160105</creationdate><title>GDF15 promotes EMT and metastasis in colorectal cancer</title><author>Li, Chen ; Wang, Jingyu ; Kong, Jianlu ; Tang, Jinlong ; Wu, Yihua ; Xu, Enping ; Zhang, Honghe ; Lai, Maode</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c354t-4f882add07cad5ddf31818a2223c7fb0625eddbac0024939774d5b8ca4c5f97e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Animals</topic><topic>Cell Line, Tumor</topic><topic>Colorectal Neoplasms - genetics</topic><topic>Colorectal Neoplasms - metabolism</topic><topic>Colorectal Neoplasms - pathology</topic><topic>Epithelial-Mesenchymal Transition - genetics</topic><topic>Female</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Growth Differentiation Factor 15 - blood</topic><topic>Growth Differentiation Factor 15 - genetics</topic><topic>Growth Differentiation Factor 15 - metabolism</topic><topic>HEK293 Cells</topic><topic>HT29 Cells</topic><topic>Humans</topic><topic>Immunoblotting</topic><topic>Immunohistochemistry</topic><topic>Male</topic><topic>Mice, Inbred NOD</topic><topic>Mice, SCID</topic><topic>Middle Aged</topic><topic>Neoplasm Metastasis</topic><topic>Proportional Hazards Models</topic><topic>Receptors, Transforming Growth Factor beta - genetics</topic><topic>Receptors, Transforming Growth Factor beta - metabolism</topic><topic>Research Paper</topic><topic>Reverse Transcriptase Polymerase Chain Reaction - statistics & numerical data</topic><topic>RNA Interference</topic><topic>Smad2 Protein - genetics</topic><topic>Smad2 Protein - metabolism</topic><topic>Smad3 Protein - genetics</topic><topic>Smad3 Protein - metabolism</topic><topic>Survival Analysis</topic><topic>Transplantation, Heterologous</topic><toplevel>online_resources</toplevel><creatorcontrib>Li, Chen</creatorcontrib><creatorcontrib>Wang, Jingyu</creatorcontrib><creatorcontrib>Kong, Jianlu</creatorcontrib><creatorcontrib>Tang, Jinlong</creatorcontrib><creatorcontrib>Wu, Yihua</creatorcontrib><creatorcontrib>Xu, Enping</creatorcontrib><creatorcontrib>Zhang, Honghe</creatorcontrib><creatorcontrib>Lai, Maode</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oncotarget</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Chen</au><au>Wang, Jingyu</au><au>Kong, Jianlu</au><au>Tang, Jinlong</au><au>Wu, Yihua</au><au>Xu, Enping</au><au>Zhang, Honghe</au><au>Lai, Maode</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>GDF15 promotes EMT and metastasis in colorectal cancer</atitle><jtitle>Oncotarget</jtitle><addtitle>Oncotarget</addtitle><date>2016-01-05</date><risdate>2016</risdate><volume>7</volume><issue>1</issue><spage>860</spage><epage>872</epage><pages>860-872</pages><issn>1949-2553</issn><eissn>1949-2553</eissn><abstract>Metastasis is the major cause of cancer deaths, and the epithelial-mesenchymal transition (EMT) has been considered to be a fundamental event in cancer metastasis. However, the role of growth differentiation factor 15 (GDF15) in colorectal cancer (CRC) metastasis and EMT remains poorly understood. Here, we showed that GDF15 promoted CRC cell metastasis both in vitro and in vivo. In addition, the EMT process was enhanced by GDF15 through binding to TGF-β receptor to activate Smad2 and Smad3 pathways. Clinical data showed GDF15 level in tumor tissues, and the serum was significantly increased, in which high GDF15 level correlated with a reduced overall survival in CRC. Thus, GDF15 may promote colorectal cancer metastasis through activating EMT. Promisingly, GDF15 could be considered as a novel prognostic marker for CRC in the clinic.</abstract><cop>United States</cop><pub>Impact Journals LLC</pub><pmid>26497212</pmid><doi>10.18632/oncotarget.6205</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Cell Line, Tumor Colorectal Neoplasms - genetics Colorectal Neoplasms - metabolism Colorectal Neoplasms - pathology Epithelial-Mesenchymal Transition - genetics Female Gene Expression Regulation, Neoplastic Growth Differentiation Factor 15 - blood Growth Differentiation Factor 15 - genetics Growth Differentiation Factor 15 - metabolism HEK293 Cells HT29 Cells Humans Immunoblotting Immunohistochemistry Male Mice, Inbred NOD Mice, SCID Middle Aged Neoplasm Metastasis Proportional Hazards Models Receptors, Transforming Growth Factor beta - genetics Receptors, Transforming Growth Factor beta - metabolism Research Paper Reverse Transcriptase Polymerase Chain Reaction - statistics & numerical data RNA Interference Smad2 Protein - genetics Smad2 Protein - metabolism Smad3 Protein - genetics Smad3 Protein - metabolism Survival Analysis Transplantation, Heterologous |
| title | GDF15 promotes EMT and metastasis in colorectal cancer |
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