Fluid shear stress induces epithelial-mesenchymal transition (EMT) in Hep-2 cells
Laryngeal squamous cell carcinoma (LSCC) is one of the most commonly diagnosed malignancies with high occurrence of tumor metastasis, which usually exposes to fluid shear stress (FSS) in lymphatic channel and blood vessel. Epithelial-mesenchymal transition (EMT) is an important mechanism that induce...
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description | Laryngeal squamous cell carcinoma (LSCC) is one of the most commonly diagnosed malignancies with high occurrence of tumor metastasis, which usually exposes to fluid shear stress (FSS) in lymphatic channel and blood vessel. Epithelial-mesenchymal transition (EMT) is an important mechanism that induces metastasis and invasion of tumors. We hypothesized that FSS induced a progression of EMT in laryngeal squamous carcinoma. Accordingly, the Hep-2 cells were exposed to 1.4 dyn/cm2 FSS for different durations. Our results showed that most of cells changed their morphology from polygon to elongated spindle with well-organized F-actin and abundant lamellipodia/filopodia in protrusions. After removing the FSS, cells gradually recovered their flat polygon morphology. FSS induced Hep-2 cells to enhance their migration capacity in a time-dependent manner. In addition, FSS down-regulated E-cadherin, and simultaneously up-regulated N-cadherin, translocated β-catenin into the nucleus. These results confirmed that FSS induced the EMT in Hep-2 cells, and revealed a reversible mesenchymal-epithelial transition (MET) process when FSS was removed. We further examined the time-expressions of signaling cascades, and demonstrated that FSS induces the EMT and enhances cell migration depending on integrin-ILK/PI3K-AKT-Snail signaling events. The current study suggests that FSS, an important biophysical factor in tumor microenvironment, is a potential determinant of cell behavior and function regulation. |
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Epithelial-mesenchymal transition (EMT) is an important mechanism that induces metastasis and invasion of tumors. We hypothesized that FSS induced a progression of EMT in laryngeal squamous carcinoma. Accordingly, the Hep-2 cells were exposed to 1.4 dyn/cm2 FSS for different durations. Our results showed that most of cells changed their morphology from polygon to elongated spindle with well-organized F-actin and abundant lamellipodia/filopodia in protrusions. After removing the FSS, cells gradually recovered their flat polygon morphology. FSS induced Hep-2 cells to enhance their migration capacity in a time-dependent manner. In addition, FSS down-regulated E-cadherin, and simultaneously up-regulated N-cadherin, translocated β-catenin into the nucleus. These results confirmed that FSS induced the EMT in Hep-2 cells, and revealed a reversible mesenchymal-epithelial transition (MET) process when FSS was removed. We further examined the time-expressions of signaling cascades, and demonstrated that FSS induces the EMT and enhances cell migration depending on integrin-ILK/PI3K-AKT-Snail signaling events. The current study suggests that FSS, an important biophysical factor in tumor microenvironment, is a potential determinant of cell behavior and function regulation.</description><identifier>ISSN: 1949-2553</identifier><identifier>EISSN: 1949-2553</identifier><identifier>DOI: 10.18632/oncotarget.8765</identifier><identifier>PMID: 27096955</identifier><language>eng</language><publisher>United States: Impact Journals LLC</publisher><subject>Antigens, CD - metabolism ; beta Catenin - metabolism ; Cadherins - metabolism ; Carcinoma, Squamous Cell - genetics ; Carcinoma, Squamous Cell - metabolism ; Carcinoma, Squamous Cell - pathology ; Cell Line, Tumor ; Cell Movement ; Cell Shape ; Epithelial-Mesenchymal Transition ; Head and Neck Neoplasms - genetics ; Head and Neck Neoplasms - metabolism ; Head and Neck Neoplasms - pathology ; Humans ; Laryngeal Neoplasms - genetics ; Laryngeal Neoplasms - metabolism ; Laryngeal Neoplasms - pathology ; Mechanotransduction, Cellular ; Phosphatidylinositol 3-Kinase - metabolism ; Protein-Serine-Threonine Kinases - metabolism ; Proto-Oncogene Proteins c-akt - metabolism ; Pseudopodia - metabolism ; Pseudopodia - pathology ; Research Paper ; RNA Interference ; Snail Family Transcription Factors - genetics ; Snail Family Transcription Factors - metabolism ; Squamous Cell Carcinoma of Head and Neck ; Stress, Mechanical ; Time Factors ; Transfection ; Tumor Microenvironment</subject><ispartof>Oncotarget, 2016-05, Vol.7 (22), p.32876-32892</ispartof><rights>Copyright: © 2016 Liu et al. 2016</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c354t-c30a27daa49a34b1dbbe14ef90ff9af437f5b5e966c725a827db40fc41b9701f3</citedby><cites>FETCH-LOGICAL-c354t-c30a27daa49a34b1dbbe14ef90ff9af437f5b5e966c725a827db40fc41b9701f3</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/PMC5078059/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5078059/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27096955$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Shuangfeng</creatorcontrib><creatorcontrib>Zhou, Fating</creatorcontrib><creatorcontrib>Shen, Yang</creatorcontrib><creatorcontrib>Zhang, Yingying</creatorcontrib><creatorcontrib>Yin, Hongmei</creatorcontrib><creatorcontrib>Zeng, Ye</creatorcontrib><creatorcontrib>Liu, Jingxia</creatorcontrib><creatorcontrib>Yan, Zhiping</creatorcontrib><creatorcontrib>Liu, Xiaoheng</creatorcontrib><title>Fluid shear stress induces epithelial-mesenchymal transition (EMT) in Hep-2 cells</title><title>Oncotarget</title><addtitle>Oncotarget</addtitle><description>Laryngeal squamous cell carcinoma (LSCC) is one of the most commonly diagnosed malignancies with high occurrence of tumor metastasis, which usually exposes to fluid shear stress (FSS) in lymphatic channel and blood vessel. Epithelial-mesenchymal transition (EMT) is an important mechanism that induces metastasis and invasion of tumors. We hypothesized that FSS induced a progression of EMT in laryngeal squamous carcinoma. Accordingly, the Hep-2 cells were exposed to 1.4 dyn/cm2 FSS for different durations. Our results showed that most of cells changed their morphology from polygon to elongated spindle with well-organized F-actin and abundant lamellipodia/filopodia in protrusions. After removing the FSS, cells gradually recovered their flat polygon morphology. FSS induced Hep-2 cells to enhance their migration capacity in a time-dependent manner. In addition, FSS down-regulated E-cadherin, and simultaneously up-regulated N-cadherin, translocated β-catenin into the nucleus. These results confirmed that FSS induced the EMT in Hep-2 cells, and revealed a reversible mesenchymal-epithelial transition (MET) process when FSS was removed. We further examined the time-expressions of signaling cascades, and demonstrated that FSS induces the EMT and enhances cell migration depending on integrin-ILK/PI3K-AKT-Snail signaling events. The current study suggests that FSS, an important biophysical factor in tumor microenvironment, is a potential determinant of cell behavior and function regulation.</description><subject>Antigens, CD - metabolism</subject><subject>beta Catenin - metabolism</subject><subject>Cadherins - metabolism</subject><subject>Carcinoma, Squamous Cell - genetics</subject><subject>Carcinoma, Squamous Cell - metabolism</subject><subject>Carcinoma, Squamous Cell - pathology</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement</subject><subject>Cell Shape</subject><subject>Epithelial-Mesenchymal Transition</subject><subject>Head and Neck Neoplasms - genetics</subject><subject>Head and Neck Neoplasms - metabolism</subject><subject>Head and Neck Neoplasms - pathology</subject><subject>Humans</subject><subject>Laryngeal Neoplasms - genetics</subject><subject>Laryngeal Neoplasms - metabolism</subject><subject>Laryngeal Neoplasms - pathology</subject><subject>Mechanotransduction, Cellular</subject><subject>Phosphatidylinositol 3-Kinase - metabolism</subject><subject>Protein-Serine-Threonine Kinases - metabolism</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Pseudopodia - metabolism</subject><subject>Pseudopodia - pathology</subject><subject>Research Paper</subject><subject>RNA Interference</subject><subject>Snail Family Transcription Factors - genetics</subject><subject>Snail Family Transcription Factors - metabolism</subject><subject>Squamous Cell Carcinoma of Head and Neck</subject><subject>Stress, Mechanical</subject><subject>Time Factors</subject><subject>Transfection</subject><subject>Tumor Microenvironment</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>eNpVkd9LwzAQx4Mobsy9-yR9nA-dSZq0zYsgwzlhIsJ8Dml6WSP9MZNW2H9v5-ac95A7yOe-d8kXoWuCpySNI3rX1LpplVtDO02TmJ-hIRFMhJTz6PykHqCx9x-4D86SlIpLNKAJFrHgfIje5mVn88AXoFzgWwfeB7bOOw0-gI1tCyitKsMKPNS62FaqDFqnam9b29TB5PFlddvzwQI2IQ00lKW_QhdGlR7GhzxC7_PH1WwRLl-fnmcPy1BHnLX9iRVNcqWYUBHLSJ5lQBgYgY0RyrAoMTzjIOJYJ5SrtGczho1mJBMJJiYaofu97qbLKsg11P1ipdw4Wym3lY2y8v9NbQu5br4kx0mKuegFJgcB13x24FtZWb97gqqh6bwkKd1hMaE9iveodo33DsxxDMHyxwz5Z4bcmdG33Jyud2z4_froG5lPieU</recordid><startdate>20160531</startdate><enddate>20160531</enddate><creator>Liu, Shuangfeng</creator><creator>Zhou, Fating</creator><creator>Shen, Yang</creator><creator>Zhang, Yingying</creator><creator>Yin, Hongmei</creator><creator>Zeng, Ye</creator><creator>Liu, Jingxia</creator><creator>Yan, Zhiping</creator><creator>Liu, Xiaoheng</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>20160531</creationdate><title>Fluid shear stress induces epithelial-mesenchymal transition (EMT) in Hep-2 cells</title><author>Liu, Shuangfeng ; Zhou, Fating ; Shen, Yang ; Zhang, Yingying ; Yin, Hongmei ; Zeng, Ye ; Liu, Jingxia ; Yan, Zhiping ; Liu, Xiaoheng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c354t-c30a27daa49a34b1dbbe14ef90ff9af437f5b5e966c725a827db40fc41b9701f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Antigens, CD - metabolism</topic><topic>beta Catenin - metabolism</topic><topic>Cadherins - metabolism</topic><topic>Carcinoma, Squamous Cell - genetics</topic><topic>Carcinoma, Squamous Cell - metabolism</topic><topic>Carcinoma, Squamous Cell - pathology</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement</topic><topic>Cell Shape</topic><topic>Epithelial-Mesenchymal Transition</topic><topic>Head and Neck Neoplasms - genetics</topic><topic>Head and Neck Neoplasms - metabolism</topic><topic>Head and Neck Neoplasms - pathology</topic><topic>Humans</topic><topic>Laryngeal Neoplasms - genetics</topic><topic>Laryngeal Neoplasms - metabolism</topic><topic>Laryngeal Neoplasms - pathology</topic><topic>Mechanotransduction, Cellular</topic><topic>Phosphatidylinositol 3-Kinase - metabolism</topic><topic>Protein-Serine-Threonine Kinases - metabolism</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Pseudopodia - metabolism</topic><topic>Pseudopodia - pathology</topic><topic>Research Paper</topic><topic>RNA Interference</topic><topic>Snail Family Transcription Factors - genetics</topic><topic>Snail Family Transcription Factors - metabolism</topic><topic>Squamous Cell Carcinoma of Head and Neck</topic><topic>Stress, Mechanical</topic><topic>Time Factors</topic><topic>Transfection</topic><topic>Tumor Microenvironment</topic><toplevel>online_resources</toplevel><creatorcontrib>Liu, Shuangfeng</creatorcontrib><creatorcontrib>Zhou, Fating</creatorcontrib><creatorcontrib>Shen, Yang</creatorcontrib><creatorcontrib>Zhang, Yingying</creatorcontrib><creatorcontrib>Yin, Hongmei</creatorcontrib><creatorcontrib>Zeng, Ye</creatorcontrib><creatorcontrib>Liu, Jingxia</creatorcontrib><creatorcontrib>Yan, Zhiping</creatorcontrib><creatorcontrib>Liu, Xiaoheng</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>Liu, Shuangfeng</au><au>Zhou, Fating</au><au>Shen, Yang</au><au>Zhang, Yingying</au><au>Yin, Hongmei</au><au>Zeng, Ye</au><au>Liu, Jingxia</au><au>Yan, Zhiping</au><au>Liu, Xiaoheng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Fluid shear stress induces epithelial-mesenchymal transition (EMT) in Hep-2 cells</atitle><jtitle>Oncotarget</jtitle><addtitle>Oncotarget</addtitle><date>2016-05-31</date><risdate>2016</risdate><volume>7</volume><issue>22</issue><spage>32876</spage><epage>32892</epage><pages>32876-32892</pages><issn>1949-2553</issn><eissn>1949-2553</eissn><abstract>Laryngeal squamous cell carcinoma (LSCC) is one of the most commonly diagnosed malignancies with high occurrence of tumor metastasis, which usually exposes to fluid shear stress (FSS) in lymphatic channel and blood vessel. Epithelial-mesenchymal transition (EMT) is an important mechanism that induces metastasis and invasion of tumors. We hypothesized that FSS induced a progression of EMT in laryngeal squamous carcinoma. Accordingly, the Hep-2 cells were exposed to 1.4 dyn/cm2 FSS for different durations. Our results showed that most of cells changed their morphology from polygon to elongated spindle with well-organized F-actin and abundant lamellipodia/filopodia in protrusions. After removing the FSS, cells gradually recovered their flat polygon morphology. FSS induced Hep-2 cells to enhance their migration capacity in a time-dependent manner. In addition, FSS down-regulated E-cadherin, and simultaneously up-regulated N-cadherin, translocated β-catenin into the nucleus. These results confirmed that FSS induced the EMT in Hep-2 cells, and revealed a reversible mesenchymal-epithelial transition (MET) process when FSS was removed. We further examined the time-expressions of signaling cascades, and demonstrated that FSS induces the EMT and enhances cell migration depending on integrin-ILK/PI3K-AKT-Snail signaling events. The current study suggests that FSS, an important biophysical factor in tumor microenvironment, is a potential determinant of cell behavior and function regulation.</abstract><cop>United States</cop><pub>Impact Journals LLC</pub><pmid>27096955</pmid><doi>10.18632/oncotarget.8765</doi><tpages>17</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Antigens, CD - metabolism beta Catenin - metabolism Cadherins - metabolism Carcinoma, Squamous Cell - genetics Carcinoma, Squamous Cell - metabolism Carcinoma, Squamous Cell - pathology Cell Line, Tumor Cell Movement Cell Shape Epithelial-Mesenchymal Transition Head and Neck Neoplasms - genetics Head and Neck Neoplasms - metabolism Head and Neck Neoplasms - pathology Humans Laryngeal Neoplasms - genetics Laryngeal Neoplasms - metabolism Laryngeal Neoplasms - pathology Mechanotransduction, Cellular Phosphatidylinositol 3-Kinase - metabolism Protein-Serine-Threonine Kinases - metabolism Proto-Oncogene Proteins c-akt - metabolism Pseudopodia - metabolism Pseudopodia - pathology Research Paper RNA Interference Snail Family Transcription Factors - genetics Snail Family Transcription Factors - metabolism Squamous Cell Carcinoma of Head and Neck Stress, Mechanical Time Factors Transfection Tumor Microenvironment |
title | Fluid shear stress induces epithelial-mesenchymal transition (EMT) in Hep-2 cells |
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