Rufy3 promotes metastasis through epithelial-mesenchymal transition in colorectal cancer
Abstract Rufy3 is a RUN domain-containing protein that has been associated with gastric cancers; however, the role of Rufy3 in the progression of colorectal cancer (CRC) remains unknown. We demonstrated that Rufy3 expression was higher in 11/12 fresh CRC tissues than in adjacent normal tissues. Rufy...
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| Veröffentlicht in: | Cancer letters 2017-04, Vol.390, p.30-38 |
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| container_title | Cancer letters |
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| creator | Xie, Ruyi Wang, Jing Tang, Weimei Li, Yueqiao Peng, Ying Zhang, Hui Liu, Guangnan Huang, Xiaoting Zhao, Jinjun Li, Aimin Gong, Wei Chen, Ye Ren, Yuexin Wang, Yadong Li, Guoxin Liu, Side Wang, Jide |
| description | Abstract Rufy3 is a RUN domain-containing protein that has been associated with gastric cancers; however, the role of Rufy3 in the progression of colorectal cancer (CRC) remains unknown. We demonstrated that Rufy3 expression was higher in 11/12 fresh CRC tissues than in adjacent normal tissues. Rufy3 induced elevated expression and transactivity of four major oncogenes in CRC. Moreover, siRNA-mediated repression of Rufy3 induced G0/G1 cell cycle arrest, and Rufy3 overexpression enhanced CRC cell proliferation in vitro and in vivo. Furthermore, Rufy3 up-regulation promoted epithelial-mesenchymal transition (EMT) and metastatic phenotypes. Using an established in vitro cell model of 5-fluorouracil-resistant (5-FU) CRC cells, we assessed cellular morphology, molecular changes, and invasion and found that these characteristics were consistent with EMT. Silencing of Rufy3 by siRNA reversed EMT and greatly diminished the invasion of 5-FU-treated cells. In addition, TGF-β1 induced Rufy3 expression in a dose-dependent manner, and Rufy3 knockdown inhibited TGF-β1-induced EMT. In vivo, higher expression of Rufy3 promoted CRC cell invasion and metastasis and induced EMT. Taken together, this work identified that Rufy3 promoted cancer metastasis in CRC cells through EMT induction. |
| doi_str_mv | 10.1016/j.canlet.2017.01.001 |
| format | Article |
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We demonstrated that Rufy3 expression was higher in 11/12 fresh CRC tissues than in adjacent normal tissues. Rufy3 induced elevated expression and transactivity of four major oncogenes in CRC. Moreover, siRNA-mediated repression of Rufy3 induced G0/G1 cell cycle arrest, and Rufy3 overexpression enhanced CRC cell proliferation in vitro and in vivo. Furthermore, Rufy3 up-regulation promoted epithelial-mesenchymal transition (EMT) and metastatic phenotypes. Using an established in vitro cell model of 5-fluorouracil-resistant (5-FU) CRC cells, we assessed cellular morphology, molecular changes, and invasion and found that these characteristics were consistent with EMT. Silencing of Rufy3 by siRNA reversed EMT and greatly diminished the invasion of 5-FU-treated cells. In addition, TGF-β1 induced Rufy3 expression in a dose-dependent manner, and Rufy3 knockdown inhibited TGF-β1-induced EMT. In vivo, higher expression of Rufy3 promoted CRC cell invasion and metastasis and induced EMT. Taken together, this work identified that Rufy3 promoted cancer metastasis in CRC cells through EMT induction.</description><identifier>ISSN: 0304-3835</identifier><identifier>EISSN: 1872-7980</identifier><identifier>DOI: 10.1016/j.canlet.2017.01.001</identifier><identifier>PMID: 28089833</identifier><language>eng</language><publisher>Ireland: Elsevier B.V</publisher><subject>Breast cancer ; Cloning ; Colorectal cancer ; Colorectal Neoplasms - genetics ; Colorectal Neoplasms - physiopathology ; Epithelial-Mesenchymal Transition - genetics ; Epithelial–mesenchymal transition ; Gastroenterology ; Genes ; Hematology, Oncology and Palliative Medicine ; Hospitals ; Humans ; Kinases ; Laboratory animals ; Metastasis ; Methods ; Models, Biological ; Mortality ; Neoplasm Metastasis - genetics ; Plasmids ; Prognosis ; Proteins ; rab5 GTP-Binding Proteins - metabolism ; Rufy3 ; Studies ; TGF-β1 ; Transcription factors</subject><ispartof>Cancer letters, 2017-04, Vol.390, p.30-38</ispartof><rights>2017 Elsevier B.V.</rights><rights>Copyright © 2017 Elsevier B.V. All rights reserved.</rights><rights>Copyright Elsevier Limited Apr 1, 2017</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c478t-e448f080ecc0481ea7919d3b17dddf8b1691deb03c4b3f6c70d0d002c41266333</citedby><cites>FETCH-LOGICAL-c478t-e448f080ecc0481ea7919d3b17dddf8b1691deb03c4b3f6c70d0d002c41266333</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.canlet.2017.01.001$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3549,27923,27924,45994</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28089833$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Xie, Ruyi</creatorcontrib><creatorcontrib>Wang, Jing</creatorcontrib><creatorcontrib>Tang, Weimei</creatorcontrib><creatorcontrib>Li, Yueqiao</creatorcontrib><creatorcontrib>Peng, Ying</creatorcontrib><creatorcontrib>Zhang, Hui</creatorcontrib><creatorcontrib>Liu, Guangnan</creatorcontrib><creatorcontrib>Huang, Xiaoting</creatorcontrib><creatorcontrib>Zhao, Jinjun</creatorcontrib><creatorcontrib>Li, Aimin</creatorcontrib><creatorcontrib>Gong, Wei</creatorcontrib><creatorcontrib>Chen, Ye</creatorcontrib><creatorcontrib>Ren, Yuexin</creatorcontrib><creatorcontrib>Wang, Yadong</creatorcontrib><creatorcontrib>Li, Guoxin</creatorcontrib><creatorcontrib>Liu, Side</creatorcontrib><creatorcontrib>Wang, Jide</creatorcontrib><title>Rufy3 promotes metastasis through epithelial-mesenchymal transition in colorectal cancer</title><title>Cancer letters</title><addtitle>Cancer Lett</addtitle><description>Abstract Rufy3 is a RUN domain-containing protein that has been associated with gastric cancers; however, the role of Rufy3 in the progression of colorectal cancer (CRC) remains unknown. We demonstrated that Rufy3 expression was higher in 11/12 fresh CRC tissues than in adjacent normal tissues. Rufy3 induced elevated expression and transactivity of four major oncogenes in CRC. Moreover, siRNA-mediated repression of Rufy3 induced G0/G1 cell cycle arrest, and Rufy3 overexpression enhanced CRC cell proliferation in vitro and in vivo. Furthermore, Rufy3 up-regulation promoted epithelial-mesenchymal transition (EMT) and metastatic phenotypes. Using an established in vitro cell model of 5-fluorouracil-resistant (5-FU) CRC cells, we assessed cellular morphology, molecular changes, and invasion and found that these characteristics were consistent with EMT. Silencing of Rufy3 by siRNA reversed EMT and greatly diminished the invasion of 5-FU-treated cells. In addition, TGF-β1 induced Rufy3 expression in a dose-dependent manner, and Rufy3 knockdown inhibited TGF-β1-induced EMT. In vivo, higher expression of Rufy3 promoted CRC cell invasion and metastasis and induced EMT. Taken together, this work identified that Rufy3 promoted cancer metastasis in CRC cells through EMT induction.</description><subject>Breast cancer</subject><subject>Cloning</subject><subject>Colorectal cancer</subject><subject>Colorectal Neoplasms - genetics</subject><subject>Colorectal Neoplasms - physiopathology</subject><subject>Epithelial-Mesenchymal Transition - genetics</subject><subject>Epithelial–mesenchymal transition</subject><subject>Gastroenterology</subject><subject>Genes</subject><subject>Hematology, Oncology and Palliative Medicine</subject><subject>Hospitals</subject><subject>Humans</subject><subject>Kinases</subject><subject>Laboratory animals</subject><subject>Metastasis</subject><subject>Methods</subject><subject>Models, Biological</subject><subject>Mortality</subject><subject>Neoplasm Metastasis - genetics</subject><subject>Plasmids</subject><subject>Prognosis</subject><subject>Proteins</subject><subject>rab5 GTP-Binding Proteins - metabolism</subject><subject>Rufy3</subject><subject>Studies</subject><subject>TGF-β1</subject><subject>Transcription factors</subject><issn>0304-3835</issn><issn>1872-7980</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkk2L1TAUhoMoznX0H4gU3LhpPadpm3QjyDB-wIDgB7gLaXrqzTVtrkkq3H9vyh0VZqMkkEWe8_W-h7GnCBUCdi8PldGLo1TVgKICrADwHtuhFHUpegn32Q44NCWXvL1gj2I8AEDbiPYhu6glyF5yvmNfP67TiRfH4GefKBYzJR3ztbFI--DXb_uCjjbtyVntypkiLWZ_mrUrUtBLtMn6pbBLYbzzgUzKH7ktQ-ExezBpF-nJ7XvJvry5_nz1rrz58Pb91eub0jRCppKaRk4ggYyBRiJp0WM_8gHFOI6THLDrcaQBuGkGPnVGwJgP1KbBuus455fsxTlvHuHHSjGp2UZDzumF_BrVpoese17L_0A7bGsEITL6_A568GtY8iAblXsElJip5kyZ4GMMNKljsLMOJ4WgNpPUQZ1NUptJClBlk3LYs9vk6zDT-CfotysZeHUGKAv301JQ0dgsPI1201iN3v6rwt0ExtnFGu2-04ni31lUrBWoT9uibHuCgufwFvgvroa5Uw</recordid><startdate>20170401</startdate><enddate>20170401</enddate><creator>Xie, Ruyi</creator><creator>Wang, Jing</creator><creator>Tang, Weimei</creator><creator>Li, Yueqiao</creator><creator>Peng, Ying</creator><creator>Zhang, Hui</creator><creator>Liu, Guangnan</creator><creator>Huang, Xiaoting</creator><creator>Zhao, Jinjun</creator><creator>Li, Aimin</creator><creator>Gong, Wei</creator><creator>Chen, Ye</creator><creator>Ren, Yuexin</creator><creator>Wang, Yadong</creator><creator>Li, Guoxin</creator><creator>Liu, Side</creator><creator>Wang, Jide</creator><general>Elsevier B.V</general><general>Elsevier Limited</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>7TO</scope><scope>7U9</scope><scope>H94</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope></search><sort><creationdate>20170401</creationdate><title>Rufy3 promotes metastasis through epithelial-mesenchymal transition in colorectal cancer</title><author>Xie, Ruyi ; Wang, Jing ; Tang, Weimei ; Li, Yueqiao ; Peng, Ying ; Zhang, Hui ; Liu, Guangnan ; Huang, Xiaoting ; Zhao, Jinjun ; Li, Aimin ; Gong, Wei ; Chen, Ye ; Ren, Yuexin ; Wang, Yadong ; Li, Guoxin ; Liu, Side ; Wang, Jide</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c478t-e448f080ecc0481ea7919d3b17dddf8b1691deb03c4b3f6c70d0d002c41266333</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Breast cancer</topic><topic>Cloning</topic><topic>Colorectal cancer</topic><topic>Colorectal Neoplasms - genetics</topic><topic>Colorectal Neoplasms - physiopathology</topic><topic>Epithelial-Mesenchymal Transition - genetics</topic><topic>Epithelial–mesenchymal transition</topic><topic>Gastroenterology</topic><topic>Genes</topic><topic>Hematology, Oncology and Palliative Medicine</topic><topic>Hospitals</topic><topic>Humans</topic><topic>Kinases</topic><topic>Laboratory animals</topic><topic>Metastasis</topic><topic>Methods</topic><topic>Models, Biological</topic><topic>Mortality</topic><topic>Neoplasm Metastasis - genetics</topic><topic>Plasmids</topic><topic>Prognosis</topic><topic>Proteins</topic><topic>rab5 GTP-Binding Proteins - metabolism</topic><topic>Rufy3</topic><topic>Studies</topic><topic>TGF-β1</topic><topic>Transcription factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Xie, Ruyi</creatorcontrib><creatorcontrib>Wang, Jing</creatorcontrib><creatorcontrib>Tang, Weimei</creatorcontrib><creatorcontrib>Li, Yueqiao</creatorcontrib><creatorcontrib>Peng, Ying</creatorcontrib><creatorcontrib>Zhang, Hui</creatorcontrib><creatorcontrib>Liu, Guangnan</creatorcontrib><creatorcontrib>Huang, Xiaoting</creatorcontrib><creatorcontrib>Zhao, Jinjun</creatorcontrib><creatorcontrib>Li, Aimin</creatorcontrib><creatorcontrib>Gong, Wei</creatorcontrib><creatorcontrib>Chen, Ye</creatorcontrib><creatorcontrib>Ren, Yuexin</creatorcontrib><creatorcontrib>Wang, Yadong</creatorcontrib><creatorcontrib>Li, Guoxin</creatorcontrib><creatorcontrib>Liu, Side</creatorcontrib><creatorcontrib>Wang, Jide</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Cancer letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Xie, Ruyi</au><au>Wang, Jing</au><au>Tang, Weimei</au><au>Li, Yueqiao</au><au>Peng, Ying</au><au>Zhang, Hui</au><au>Liu, Guangnan</au><au>Huang, Xiaoting</au><au>Zhao, Jinjun</au><au>Li, Aimin</au><au>Gong, Wei</au><au>Chen, Ye</au><au>Ren, Yuexin</au><au>Wang, Yadong</au><au>Li, Guoxin</au><au>Liu, Side</au><au>Wang, Jide</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Rufy3 promotes metastasis through epithelial-mesenchymal transition in colorectal cancer</atitle><jtitle>Cancer letters</jtitle><addtitle>Cancer Lett</addtitle><date>2017-04-01</date><risdate>2017</risdate><volume>390</volume><spage>30</spage><epage>38</epage><pages>30-38</pages><issn>0304-3835</issn><eissn>1872-7980</eissn><abstract>Abstract Rufy3 is a RUN domain-containing protein that has been associated with gastric cancers; however, the role of Rufy3 in the progression of colorectal cancer (CRC) remains unknown. We demonstrated that Rufy3 expression was higher in 11/12 fresh CRC tissues than in adjacent normal tissues. Rufy3 induced elevated expression and transactivity of four major oncogenes in CRC. Moreover, siRNA-mediated repression of Rufy3 induced G0/G1 cell cycle arrest, and Rufy3 overexpression enhanced CRC cell proliferation in vitro and in vivo. Furthermore, Rufy3 up-regulation promoted epithelial-mesenchymal transition (EMT) and metastatic phenotypes. Using an established in vitro cell model of 5-fluorouracil-resistant (5-FU) CRC cells, we assessed cellular morphology, molecular changes, and invasion and found that these characteristics were consistent with EMT. Silencing of Rufy3 by siRNA reversed EMT and greatly diminished the invasion of 5-FU-treated cells. In addition, TGF-β1 induced Rufy3 expression in a dose-dependent manner, and Rufy3 knockdown inhibited TGF-β1-induced EMT. In vivo, higher expression of Rufy3 promoted CRC cell invasion and metastasis and induced EMT. Taken together, this work identified that Rufy3 promoted cancer metastasis in CRC cells through EMT induction.</abstract><cop>Ireland</cop><pub>Elsevier B.V</pub><pmid>28089833</pmid><doi>10.1016/j.canlet.2017.01.001</doi><tpages>9</tpages></addata></record> |
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| subjects | Breast cancer Cloning Colorectal cancer Colorectal Neoplasms - genetics Colorectal Neoplasms - physiopathology Epithelial-Mesenchymal Transition - genetics Epithelial–mesenchymal transition Gastroenterology Genes Hematology, Oncology and Palliative Medicine Hospitals Humans Kinases Laboratory animals Metastasis Methods Models, Biological Mortality Neoplasm Metastasis - genetics Plasmids Prognosis Proteins rab5 GTP-Binding Proteins - metabolism Rufy3 Studies TGF-β1 Transcription factors |
| title | Rufy3 promotes metastasis through epithelial-mesenchymal transition in colorectal cancer |
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