ARK5 is associated with the invasive and metastatic potential of human breast cancer cells
Purpose To investigate the effects of Akt/ARK5 pathways on the metastatic potential of human breast cancer cells. Materials and methods The human ARK5 gene was transfected into MDA-MB-231 cells. Effects of ARK5 on MDA-MB-231 cells were investigated in vitro. The tumorigenicity and spontaneously meta...
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| Veröffentlicht in: | Journal of cancer research and clinical oncology 2012-02, Vol.138 (2), p.247-254 |
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| creator | Chang, Xin-Zhong Yu, Jie Liu, Hai-Yin Dong, Rui-Hua Cao, Xu-Chen |
| description | Purpose
To investigate the effects of Akt/ARK5 pathways on the metastatic potential of human breast cancer cells.
Materials and methods
The human ARK5 gene was transfected into MDA-MB-231 cells. Effects of ARK5 on MDA-MB-231 cells were investigated in vitro. The tumorigenicity and spontaneously metastatic capability regulated by ARK5 were determined using an orthotopic xenograft tumor model.
Results
ARK5 enhanced the invasive and metastatic potential of MDA-MB-231 cells under regulation by Akt. The enhancement was associated with increasing MMP-2, MMP-9, and MT1-MMP expression. The results were further demonstrated by RNA interference experiment. In an in vivo study, we also demonstrated that ARK5-transfected breast cancer cells grew faster and had more pulmonary metastases than its parental counterparts.
Conclusion
ARK5 led to a more invasive phenotype and metastatic potential in human breast cancer dependent on Akt. |
| doi_str_mv | 10.1007/s00432-011-1102-1 |
| format | Article |
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To investigate the effects of Akt/ARK5 pathways on the metastatic potential of human breast cancer cells.
Materials and methods
The human ARK5 gene was transfected into MDA-MB-231 cells. Effects of ARK5 on MDA-MB-231 cells were investigated in vitro. The tumorigenicity and spontaneously metastatic capability regulated by ARK5 were determined using an orthotopic xenograft tumor model.
Results
ARK5 enhanced the invasive and metastatic potential of MDA-MB-231 cells under regulation by Akt. The enhancement was associated with increasing MMP-2, MMP-9, and MT1-MMP expression. The results were further demonstrated by RNA interference experiment. In an in vivo study, we also demonstrated that ARK5-transfected breast cancer cells grew faster and had more pulmonary metastases than its parental counterparts.
Conclusion
ARK5 led to a more invasive phenotype and metastatic potential in human breast cancer dependent on Akt.</description><identifier>ISSN: 0171-5216</identifier><identifier>EISSN: 1432-1335</identifier><identifier>DOI: 10.1007/s00432-011-1102-1</identifier><identifier>PMID: 22105900</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer-Verlag</publisher><subject>Animals ; Breast cancer ; Breast Neoplasms - genetics ; Breast Neoplasms - metabolism ; Breast Neoplasms - pathology ; Cancer Research ; Cell Adhesion - genetics ; Cell Line, Tumor ; Cell Transformation, Neoplastic - genetics ; Cell Transformation, Neoplastic - metabolism ; Cell Transformation, Neoplastic - pathology ; Female ; Gene Expression Regulation, Neoplastic ; Genes ; Hematology ; Humans ; Internal Medicine ; Lung Neoplasms - genetics ; Lung Neoplasms - metabolism ; Lung Neoplasms - pathology ; Lung Neoplasms - secondary ; Matrix Metalloproteinase 14 - genetics ; Matrix Metalloproteinase 14 - metabolism ; Matrix Metalloproteinase 2 - genetics ; Matrix Metalloproteinase 2 - metabolism ; Matrix Metalloproteinase 9 - genetics ; Matrix Metalloproteinase 9 - metabolism ; Medicine ; Medicine & Public Health ; Metastasis ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Neoplasm Invasiveness ; Neoplasm Metastasis ; Oncology ; Original Paper ; Protein Kinases - genetics ; Protein Kinases - metabolism ; Proto-Oncogene Proteins c-akt - metabolism ; Repressor Proteins - genetics ; Repressor Proteins - metabolism ; RNA Interference ; Transfection - methods</subject><ispartof>Journal of cancer research and clinical oncology, 2012-02, Vol.138 (2), p.247-254</ispartof><rights>Springer-Verlag 2011</rights><rights>Springer-Verlag 2012</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c370t-cd9eab93e543bae27f58e3ef583e47829b27c38d09db075e42aceca91c8876e33</citedby><cites>FETCH-LOGICAL-c370t-cd9eab93e543bae27f58e3ef583e47829b27c38d09db075e42aceca91c8876e33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00432-011-1102-1$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00432-011-1102-1$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27903,27904,41467,42536,51297</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22105900$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chang, Xin-Zhong</creatorcontrib><creatorcontrib>Yu, Jie</creatorcontrib><creatorcontrib>Liu, Hai-Yin</creatorcontrib><creatorcontrib>Dong, Rui-Hua</creatorcontrib><creatorcontrib>Cao, Xu-Chen</creatorcontrib><title>ARK5 is associated with the invasive and metastatic potential of human breast cancer cells</title><title>Journal of cancer research and clinical oncology</title><addtitle>J Cancer Res Clin Oncol</addtitle><addtitle>J Cancer Res Clin Oncol</addtitle><description>Purpose
To investigate the effects of Akt/ARK5 pathways on the metastatic potential of human breast cancer cells.
Materials and methods
The human ARK5 gene was transfected into MDA-MB-231 cells. Effects of ARK5 on MDA-MB-231 cells were investigated in vitro. The tumorigenicity and spontaneously metastatic capability regulated by ARK5 were determined using an orthotopic xenograft tumor model.
Results
ARK5 enhanced the invasive and metastatic potential of MDA-MB-231 cells under regulation by Akt. The enhancement was associated with increasing MMP-2, MMP-9, and MT1-MMP expression. The results were further demonstrated by RNA interference experiment. In an in vivo study, we also demonstrated that ARK5-transfected breast cancer cells grew faster and had more pulmonary metastases than its parental counterparts.
Conclusion
ARK5 led to a more invasive phenotype and metastatic potential in human breast cancer dependent on Akt.</description><subject>Animals</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - metabolism</subject><subject>Breast Neoplasms - pathology</subject><subject>Cancer Research</subject><subject>Cell Adhesion - genetics</subject><subject>Cell Line, Tumor</subject><subject>Cell Transformation, Neoplastic - genetics</subject><subject>Cell Transformation, Neoplastic - metabolism</subject><subject>Cell Transformation, Neoplastic - pathology</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genes</subject><subject>Hematology</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>Lung Neoplasms - genetics</subject><subject>Lung Neoplasms - metabolism</subject><subject>Lung Neoplasms - pathology</subject><subject>Lung Neoplasms - secondary</subject><subject>Matrix Metalloproteinase 14 - genetics</subject><subject>Matrix Metalloproteinase 14 - metabolism</subject><subject>Matrix Metalloproteinase 2 - genetics</subject><subject>Matrix Metalloproteinase 2 - metabolism</subject><subject>Matrix Metalloproteinase 9 - genetics</subject><subject>Matrix Metalloproteinase 9 - metabolism</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Metastasis</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Nude</subject><subject>Neoplasm Invasiveness</subject><subject>Neoplasm Metastasis</subject><subject>Oncology</subject><subject>Original Paper</subject><subject>Protein Kinases - genetics</subject><subject>Protein Kinases - metabolism</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Repressor Proteins - genetics</subject><subject>Repressor Proteins - metabolism</subject><subject>RNA Interference</subject><subject>Transfection - methods</subject><issn>0171-5216</issn><issn>1432-1335</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp1kE9LAzEQxYMotlY_gBcJ3lczyWazOZbiPywIohcvIZudtVva3ZqkFb-9Ka168jLDzLx5D36EnAO7AsbUdWAsFzxjABkA4xkckCFsNyCEPCRDBgoyyaEYkJMQ5izNUvFjMuAcmNSMDcnb-PlR0jZQG0LvWhuxpp9tnNE4Q9p2GxvaDVLb1XSJ0YZoY-voqo_YxdYuaN_Q2XppO1p5TFfqbOfQU4eLRTglR41dBDzb9xF5vb15mdxn06e7h8l4mjmhWMxcrdFWWqDMRWWRq0aWKDBVgbkqua64cqKsma4rpiTm3Dp0VoMrS1WgECNyufNd-f5jjSGaeb_2XYo0GqQu8kLzJIKdyPk-BI-NWfl2af2XAWa2MM0OpkkwzRamgfRzsTdeV0usfz9-6CUB3wlCOnXv6P-S_3f9Bt7Afxk</recordid><startdate>20120201</startdate><enddate>20120201</enddate><creator>Chang, Xin-Zhong</creator><creator>Yu, Jie</creator><creator>Liu, Hai-Yin</creator><creator>Dong, Rui-Hua</creator><creator>Cao, Xu-Chen</creator><general>Springer-Verlag</general><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>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope></search><sort><creationdate>20120201</creationdate><title>ARK5 is associated with the invasive and metastatic potential of human breast cancer cells</title><author>Chang, Xin-Zhong ; Yu, Jie ; Liu, Hai-Yin ; Dong, Rui-Hua ; Cao, Xu-Chen</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c370t-cd9eab93e543bae27f58e3ef583e47829b27c38d09db075e42aceca91c8876e33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Animals</topic><topic>Breast cancer</topic><topic>Breast Neoplasms - genetics</topic><topic>Breast Neoplasms - metabolism</topic><topic>Breast Neoplasms - pathology</topic><topic>Cancer Research</topic><topic>Cell Adhesion - genetics</topic><topic>Cell Line, Tumor</topic><topic>Cell Transformation, Neoplastic - genetics</topic><topic>Cell Transformation, Neoplastic - metabolism</topic><topic>Cell Transformation, Neoplastic - pathology</topic><topic>Female</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genes</topic><topic>Hematology</topic><topic>Humans</topic><topic>Internal Medicine</topic><topic>Lung Neoplasms - genetics</topic><topic>Lung Neoplasms - metabolism</topic><topic>Lung Neoplasms - pathology</topic><topic>Lung Neoplasms - secondary</topic><topic>Matrix Metalloproteinase 14 - genetics</topic><topic>Matrix Metalloproteinase 14 - metabolism</topic><topic>Matrix Metalloproteinase 2 - genetics</topic><topic>Matrix Metalloproteinase 2 - metabolism</topic><topic>Matrix Metalloproteinase 9 - genetics</topic><topic>Matrix Metalloproteinase 9 - metabolism</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Metastasis</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Nude</topic><topic>Neoplasm Invasiveness</topic><topic>Neoplasm Metastasis</topic><topic>Oncology</topic><topic>Original Paper</topic><topic>Protein Kinases - genetics</topic><topic>Protein Kinases - metabolism</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Repressor Proteins - genetics</topic><topic>Repressor Proteins - metabolism</topic><topic>RNA Interference</topic><topic>Transfection - methods</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chang, Xin-Zhong</creatorcontrib><creatorcontrib>Yu, Jie</creatorcontrib><creatorcontrib>Liu, Hai-Yin</creatorcontrib><creatorcontrib>Dong, Rui-Hua</creatorcontrib><creatorcontrib>Cao, Xu-Chen</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>Oncogenes and Growth Factors 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>Public Health Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</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>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</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 Basic</collection><jtitle>Journal of cancer research and clinical oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chang, Xin-Zhong</au><au>Yu, Jie</au><au>Liu, Hai-Yin</au><au>Dong, Rui-Hua</au><au>Cao, Xu-Chen</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>ARK5 is associated with the invasive and metastatic potential of human breast cancer cells</atitle><jtitle>Journal of cancer research and clinical oncology</jtitle><stitle>J Cancer Res Clin Oncol</stitle><addtitle>J Cancer Res Clin Oncol</addtitle><date>2012-02-01</date><risdate>2012</risdate><volume>138</volume><issue>2</issue><spage>247</spage><epage>254</epage><pages>247-254</pages><issn>0171-5216</issn><eissn>1432-1335</eissn><abstract>Purpose
To investigate the effects of Akt/ARK5 pathways on the metastatic potential of human breast cancer cells.
Materials and methods
The human ARK5 gene was transfected into MDA-MB-231 cells. Effects of ARK5 on MDA-MB-231 cells were investigated in vitro. The tumorigenicity and spontaneously metastatic capability regulated by ARK5 were determined using an orthotopic xenograft tumor model.
Results
ARK5 enhanced the invasive and metastatic potential of MDA-MB-231 cells under regulation by Akt. The enhancement was associated with increasing MMP-2, MMP-9, and MT1-MMP expression. The results were further demonstrated by RNA interference experiment. In an in vivo study, we also demonstrated that ARK5-transfected breast cancer cells grew faster and had more pulmonary metastases than its parental counterparts.
Conclusion
ARK5 led to a more invasive phenotype and metastatic potential in human breast cancer dependent on Akt.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer-Verlag</pub><pmid>22105900</pmid><doi>10.1007/s00432-011-1102-1</doi><tpages>8</tpages></addata></record> |
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| subjects | Animals Breast cancer Breast Neoplasms - genetics Breast Neoplasms - metabolism Breast Neoplasms - pathology Cancer Research Cell Adhesion - genetics Cell Line, Tumor Cell Transformation, Neoplastic - genetics Cell Transformation, Neoplastic - metabolism Cell Transformation, Neoplastic - pathology Female Gene Expression Regulation, Neoplastic Genes Hematology Humans Internal Medicine Lung Neoplasms - genetics Lung Neoplasms - metabolism Lung Neoplasms - pathology Lung Neoplasms - secondary Matrix Metalloproteinase 14 - genetics Matrix Metalloproteinase 14 - metabolism Matrix Metalloproteinase 2 - genetics Matrix Metalloproteinase 2 - metabolism Matrix Metalloproteinase 9 - genetics Matrix Metalloproteinase 9 - metabolism Medicine Medicine & Public Health Metastasis Mice Mice, Inbred BALB C Mice, Nude Neoplasm Invasiveness Neoplasm Metastasis Oncology Original Paper Protein Kinases - genetics Protein Kinases - metabolism Proto-Oncogene Proteins c-akt - metabolism Repressor Proteins - genetics Repressor Proteins - metabolism RNA Interference Transfection - methods |
| title | ARK5 is associated with the invasive and metastatic potential of human breast cancer cells |
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