Down-regulation of eIF5A-2 prevents epithelial-mesenchymal transition in non-small-cell lung cancer cells

Background：Epithelial-mesenchymal transition（EMT） is believed to be the critical process in malignant tumor invasion and metastases,and has a great influence on improving the survival rate in non-small-cell lung cancer（NSCLC） patients.Recent studies suggested that eukaryotic initiation factor 5A-2（e...

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Published in:Journal of Zhejiang University. B. Science 2013-06, Vol.14 (6), p.460-467
Main Authors: Xu, Guo-dong, Shi, Xin-bao, Sun, Le-bo, Zhou, Qing-yun, Zheng, Da-wei, Shi, Huo-shun, Che, Yong-liang, Wang, Zi-shan, Shao, Guo-feng
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Language:English
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Biomedical and Life Sciences
Biomedicine
Carcinoma, Non-Small-Cell Lung - genetics
Carcinoma, Non-Small-Cell Lung - pathology
Carcinoma, Non-Small-Cell Lung - physiopathology
Cell Line, Tumor
Cell Movement - genetics
Cell Survival - genetics
Down-Regulation - genetics
Epithelial-Mesenchymal Transition - genetics
Eukaryotic Translation Initiation Factor 5A
Gene Knockdown Techniques - methods
Humans
Lung cancer
Peptide Initiation Factors - genetics
RNA-Binding Proteins - genetics
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container_end_page 467
container_issue 6
container_start_page 460
container_title Journal of Zhejiang University. B. Science
container_volume 14
creator Xu, Guo-dong
Shi, Xin-bao
Sun, Le-bo
Zhou, Qing-yun
Zheng, Da-wei
Shi, Huo-shun
Che, Yong-liang
Wang, Zi-shan
Shao, Guo-feng
description Background：Epithelial-mesenchymal transition（EMT） is believed to be the critical process in malignant tumor invasion and metastases,and has a great influence on improving the survival rate in non-small-cell lung cancer（NSCLC） patients.Recent studies suggested that eukaryotic initiation factor 5A-2（eIF5A-2） might serve as an adverse prognostic marker of survival.We detected eIF5A-2 in NSCLC A549 cells,and found that the invasive capability correlates with the eIF5A-2 expression.Methods：Transforming growth factor（TGF）-β1 was used to induce EMT in A549 cells.Western blotting,immunofluorescence,wound healing assay,and transwell-matrigel invasion chambers were used to identify phenotype changes.Western blotting was also used to observe changes of the expression of eIF5A-2.We down-regulated the eIF5A-2 expression using an eIF5A-2 siRNA and identified the phenotype changes by western blotting and immunofluorescence.We tested the change of migration and invasion capabilities of A549 cells by the wound healing assay and transwell-matrigel invasion chambers.Results：After stimulating with TGF-β1,almost all A549 cells changed to the mesenchymal phenotype and acquired more migration and invasion capabilities.These cells also had higher eIF5A-2 protein expression.Down-regulation of eIF5A-2 expression with eIF5A-2 siRNA transfection could change the cells from mesenchymal to epithelial phenotype and decrease tumor cell migration and invasive capabilities significantly.Conclusions：The expression of eIF5A-2 was up-regulated following EMT phenotype changes in A549 cells,which correlated with enhanced tumor invasion and metastatic capabilities.Furthermore,in the A549 cell line,the process of EMT phenotype change could be reversed by eIF5A-2 siRNA,with a consequent weakening of both invasive and metastatic capabilities.
doi_str_mv 10.1631/jzus.B1200200
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B</addtitle><addtitle>Journal of Zhejiang University Science</addtitle><description>Background：Epithelial-mesenchymal transition（EMT） is believed to be the critical process in malignant tumor invasion and metastases,and has a great influence on improving the survival rate in non-small-cell lung cancer（NSCLC） patients.Recent studies suggested that eukaryotic initiation factor 5A-2（eIF5A-2） might serve as an adverse prognostic marker of survival.We detected eIF5A-2 in NSCLC A549 cells,and found that the invasive capability correlates with the eIF5A-2 expression.Methods：Transforming growth factor（TGF）-β1 was used to induce EMT in A549 cells.Western blotting,immunofluorescence,wound healing assay,and transwell-matrigel invasion chambers were used to identify phenotype changes.Western blotting was also used to observe changes of the expression of eIF5A-2.We down-regulated the eIF5A-2 expression using an eIF5A-2 siRNA and identified the phenotype changes by western blotting and immunofluorescence.We tested the change of migration and invasion capabilities of A549 cells by the wound healing assay and transwell-matrigel invasion chambers.Results：After stimulating with TGF-β1,almost all A549 cells changed to the mesenchymal phenotype and acquired more migration and invasion capabilities.These cells also had higher eIF5A-2 protein expression.Down-regulation of eIF5A-2 expression with eIF5A-2 siRNA transfection could change the cells from mesenchymal to epithelial phenotype and decrease tumor cell migration and invasive capabilities significantly.Conclusions：The expression of eIF5A-2 was up-regulated following EMT phenotype changes in A549 cells,which correlated with enhanced tumor invasion and metastatic capabilities.Furthermore,in the A549 cell line,the process of EMT phenotype change could be reversed by eIF5A-2 siRNA,with a consequent weakening of both invasive and metastatic capabilities.</description><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Carcinoma, Non-Small-Cell Lung - 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genetics</topic><topic>Carcinoma, Non-Small-Cell Lung - pathology</topic><topic>Carcinoma, Non-Small-Cell Lung - physiopathology</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement - genetics</topic><topic>Cell Survival - genetics</topic><topic>Down-Regulation - genetics</topic><topic>Epithelial-Mesenchymal Transition - genetics</topic><topic>Eukaryotic Translation Initiation Factor 5A</topic><topic>Gene Knockdown Techniques - methods</topic><topic>Humans</topic><topic>Lung cancer</topic><topic>Peptide Initiation Factors - genetics</topic><topic>RNA-Binding Proteins - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Xu, Guo-dong</creatorcontrib><creatorcontrib>Shi, Xin-bao</creatorcontrib><creatorcontrib>Sun, Le-bo</creatorcontrib><creatorcontrib>Zhou, Qing-yun</creatorcontrib><creatorcontrib>Zheng, Da-wei</creatorcontrib><creatorcontrib>Shi, Huo-shun</creatorcontrib><creatorcontrib>Che, Yong-liang</creatorcontrib><creatorcontrib>Wang, Zi-shan</creatorcontrib><creatorcontrib>Shao, Guo-feng</creatorcontrib><collection>维普_期刊</collection><collection>中文科技期刊数据库-CALIS站点</collection><collection>中文科技期刊数据库-7.0平台</collection><collection>中文科技期刊数据库- 镜像站点</collection><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>Biotechnology Research Abstracts</collection><collection>Calcium &amp; Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health &amp; Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology 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>Materials Science &amp; Engineering Collection</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>Advanced Technologies &amp; Aerospace Collection</collection><collection>Agricultural &amp; Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Earth, Atmospheric &amp; Aquatic Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</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 &amp; Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>ProQuest Engineering Collection</collection><collection>Biological Sciences</collection><collection>Agriculture Science Database</collection><collection>Health &amp; Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Engineering Database</collection><collection>Advanced Technologies &amp; Aerospace Database</collection><collection>ProQuest Advanced Technologies &amp; Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>Earth, Atmospheric &amp; Aquatic Science Database</collection><collection>Materials Science Collection</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>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of Zhejiang University. B. Science</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Xu, Guo-dong</au><au>Shi, Xin-bao</au><au>Sun, Le-bo</au><au>Zhou, Qing-yun</au><au>Zheng, Da-wei</au><au>Shi, Huo-shun</au><au>Che, Yong-liang</au><au>Wang, Zi-shan</au><au>Shao, Guo-feng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Down-regulation of eIF5A-2 prevents epithelial-mesenchymal transition in non-small-cell lung cancer cells</atitle><jtitle>Journal of Zhejiang University. B. Science</jtitle><stitle>J. Zhejiang Univ. Sci. B</stitle><addtitle>Journal of Zhejiang University Science</addtitle><date>2013-06-01</date><risdate>2013</risdate><volume>14</volume><issue>6</issue><spage>460</spage><epage>467</epage><pages>460-467</pages><issn>1673-1581</issn><eissn>1862-1783</eissn><notes>Non-small-cell lung cancer（NSCLC）； Epithelial-mesenchymal transition（EMT）； Eukaryotic initiation factor 5A-2（eIF5A-2）； Transforming growth factor（TGF）-β1； A549</notes><notes>33-1356/Q</notes><notes>Background：Epithelial-mesenchymal transition（EMT） is believed to be the critical process in malignant tumor invasion and metastases,and has a great influence on improving the survival rate in non-small-cell lung cancer（NSCLC） patients.Recent studies suggested that eukaryotic initiation factor 5A-2（eIF5A-2） might serve as an adverse prognostic marker of survival.We detected eIF5A-2 in NSCLC A549 cells,and found that the invasive capability correlates with the eIF5A-2 expression.Methods：Transforming growth factor（TGF）-β1 was used to induce EMT in A549 cells.Western blotting,immunofluorescence,wound healing assay,and transwell-matrigel invasion chambers were used to identify phenotype changes.Western blotting was also used to observe changes of the expression of eIF5A-2.We down-regulated the eIF5A-2 expression using an eIF5A-2 siRNA and identified the phenotype changes by western blotting and immunofluorescence.We tested the change of migration and invasion capabilities of A549 cells by the wound healing assay and transwell-matrigel invasion chambers.Results：After stimulating with TGF-β1,almost all A549 cells changed to the mesenchymal phenotype and acquired more migration and invasion capabilities.These cells also had higher eIF5A-2 protein expression.Down-regulation of eIF5A-2 expression with eIF5A-2 siRNA transfection could change the cells from mesenchymal to epithelial phenotype and decrease tumor cell migration and invasive capabilities significantly.Conclusions：The expression of eIF5A-2 was up-regulated following EMT phenotype changes in A549 cells,which correlated with enhanced tumor invasion and metastatic capabilities.Furthermore,in the A549 cell line,the process of EMT phenotype change could be reversed by eIF5A-2 siRNA,with a consequent weakening of both invasive and metastatic capabilities.</notes><notes>ObjectType-Article-1</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-2</notes><notes>content type line 23</notes><notes>Corresponding Author</notes><abstract>Background：Epithelial-mesenchymal transition（EMT） is believed to be the critical process in malignant tumor invasion and metastases,and has a great influence on improving the survival rate in non-small-cell lung cancer（NSCLC） patients.Recent studies suggested that eukaryotic initiation factor 5A-2（eIF5A-2） might serve as an adverse prognostic marker of survival.We detected eIF5A-2 in NSCLC A549 cells,and found that the invasive capability correlates with the eIF5A-2 expression.Methods：Transforming growth factor（TGF）-β1 was used to induce EMT in A549 cells.Western blotting,immunofluorescence,wound healing assay,and transwell-matrigel invasion chambers were used to identify phenotype changes.Western blotting was also used to observe changes of the expression of eIF5A-2.We down-regulated the eIF5A-2 expression using an eIF5A-2 siRNA and identified the phenotype changes by western blotting and immunofluorescence.We tested the change of migration and invasion capabilities of A549 cells by the wound healing assay and transwell-matrigel invasion chambers.Results：After stimulating with TGF-β1,almost all A549 cells changed to the mesenchymal phenotype and acquired more migration and invasion capabilities.These cells also had higher eIF5A-2 protein expression.Down-regulation of eIF5A-2 expression with eIF5A-2 siRNA transfection could change the cells from mesenchymal to epithelial phenotype and decrease tumor cell migration and invasive capabilities significantly.Conclusions：The expression of eIF5A-2 was up-regulated following EMT phenotype changes in A549 cells,which correlated with enhanced tumor invasion and metastatic capabilities.Furthermore,in the A549 cell line,the process of EMT phenotype change could be reversed by eIF5A-2 siRNA,with a consequent weakening of both invasive and metastatic capabilities.</abstract><cop>Heidelberg</cop><pub>SP Zhejiang University Press</pub><pmid>23733422</pmid><doi>10.1631/jzus.B1200200</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record>
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source Full-Text Journals in Chemistry (Open access); Springer Link; PubMed Central
subjects Biomedical and Life Sciences
Biomedicine
Carcinoma, Non-Small-Cell Lung - genetics
Carcinoma, Non-Small-Cell Lung - pathology
Carcinoma, Non-Small-Cell Lung - physiopathology
Cell Line, Tumor
Cell Movement - genetics
Cell Survival - genetics
Down-Regulation - genetics
Epithelial-Mesenchymal Transition - genetics
Eukaryotic Translation Initiation Factor 5A
Gene Knockdown Techniques - methods
Humans
Lung cancer
Peptide Initiation Factors - genetics
RNA-Binding Proteins - genetics
title Down-regulation of eIF5A-2 prevents epithelial-mesenchymal transition in non-small-cell lung cancer cells
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