Plectin deficiency in liver cancer cells promotes cell migration and sensitivity to sorafenib treatment
Plectin involved in activation of kinases in cell signaling pathway and plays important role in cell morphology and migration. Plectin knockdown promotes cell migration by activating focal adhesion kinase and Rac1-GTPase activity in liver cells. Sorafenib is a multi-targeting tyrosine kinase inhibit...
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| Veröffentlicht in: | Cell adhesion & migration 2018-01, Vol.12 (1), p.19-27 |
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| creator | Cheng, Chiung-Chi Chao, Wei-Ting Liao, Chen-Chun Tseng, Yu-Hui Lai, Yen-Chang Clark Lai, Yih-Shyong Hsu, Yung-Hsiang Liu, Yi-Hsiang |
| description | Plectin involved in activation of kinases in cell signaling pathway and plays important role in cell morphology and migration. Plectin knockdown promotes cell migration by activating focal adhesion kinase and Rac1-GTPase activity in liver cells. Sorafenib is a multi-targeting tyrosine kinase inhibitor that improves patient survival on hepatocellular carcinoma. The aim of this study is to investigate the correlation between the expression of plectin and cell migration as well as the sensitivity of hepatoma cell lines exposing to sorafenib. Hepatoma cell lines PLC/PRF/5 and HepG2 were used to examine the level of plectin expression and cell migration in comparison with Chang liver cell line. In addition, sensitivity of the 3 cell lines to sorafenib treatment was also measured. Expression of plectin was lower in PLC/PRF/5 and HepG2 hepatoma cells than that of Chang liver cells whereas HepG2 and PLC/PRF/5 cells exhibit higher rate of cell migration in trans-well migration assay. Immunohistofluorecent staining on E-cadherin revealed the highest rate of collective cell migration in HepG2 cells and the lowest was found in Chang liver cells. Likewise, HepG2 cell line was most sensitive to sorafenib treatment and Chang liver cells exhibited the least sensitivity. The drug sensitivity to sorafenib treatment showed inverse correlation with the expression of plectin. We suggest that plectin deficiency and increased E-cadherin in hepatoma cells were associated with higher rates of cell motility, collective cell migration as well as higher drug sensitivity to sorafenib treatment. |
| doi_str_mv | 10.1080/19336918.2017.1288789 |
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Plectin knockdown promotes cell migration by activating focal adhesion kinase and Rac1-GTPase activity in liver cells. Sorafenib is a multi-targeting tyrosine kinase inhibitor that improves patient survival on hepatocellular carcinoma. The aim of this study is to investigate the correlation between the expression of plectin and cell migration as well as the sensitivity of hepatoma cell lines exposing to sorafenib. Hepatoma cell lines PLC/PRF/5 and HepG2 were used to examine the level of plectin expression and cell migration in comparison with Chang liver cell line. In addition, sensitivity of the 3 cell lines to sorafenib treatment was also measured. Expression of plectin was lower in PLC/PRF/5 and HepG2 hepatoma cells than that of Chang liver cells whereas HepG2 and PLC/PRF/5 cells exhibit higher rate of cell migration in trans-well migration assay. Immunohistofluorecent staining on E-cadherin revealed the highest rate of collective cell migration in HepG2 cells and the lowest was found in Chang liver cells. Likewise, HepG2 cell line was most sensitive to sorafenib treatment and Chang liver cells exhibited the least sensitivity. The drug sensitivity to sorafenib treatment showed inverse correlation with the expression of plectin. We suggest that plectin deficiency and increased E-cadherin in hepatoma cells were associated with higher rates of cell motility, collective cell migration as well as higher drug sensitivity to sorafenib treatment.</description><identifier>ISSN: 1933-6918</identifier><identifier>EISSN: 1933-6926</identifier><identifier>DOI: 10.1080/19336918.2017.1288789</identifier><identifier>PMID: 28276928</identifier><language>eng</language><publisher>United States: Taylor & Francis</publisher><subject>Antineoplastic Agents - therapeutic use ; Apoptosis - drug effects ; Carcinoma, Hepatocellular - drug therapy ; Carcinoma, Hepatocellular - metabolism ; Cell Line, Tumor ; Cell Movement - drug effects ; Cell Proliferation - drug effects ; Cell Survival - drug effects ; collective cell migration ; cytoskeleton ; E-cadherin ; Hep G2 Cells ; hepatocellular carcinoma ; Humans ; Liver Neoplasms - drug therapy ; Liver Neoplasms - metabolism ; Liver Neoplasms - pathology ; plectin ; Plectin - deficiency ; Protein Kinase Inhibitors - pharmacology ; Research Paper ; Signal Transduction - drug effects ; sorafenib ; Sorafenib - pharmacology</subject><ispartof>Cell adhesion & migration, 2018-01, Vol.12 (1), p.19-27</ispartof><rights>2018 The Author(s). Published with license by Taylor & Francis © 2017 Chiung-Chi Cheng, Wei-Ting Chao, Chen-Chun Liao, Yu-Hui Tseng, Yen-Chang Clark Lai, Yih-Shyong Lai, Yung-Hsiang Hsu, and Yi-Hsiang Liu 2018</rights><rights>2018 The Author(s). Published with license by Taylor & Francis 2018 The Author(s)</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c468t-f11ef48c5c76278e572b51246811883ae2fe78048276663ee56d84e11e41c9ce3</citedby><cites>FETCH-LOGICAL-c468t-f11ef48c5c76278e572b51246811883ae2fe78048276663ee56d84e11e41c9ce3</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/PMC5810502/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5810502/$$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/28276928$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cheng, Chiung-Chi</creatorcontrib><creatorcontrib>Chao, Wei-Ting</creatorcontrib><creatorcontrib>Liao, Chen-Chun</creatorcontrib><creatorcontrib>Tseng, Yu-Hui</creatorcontrib><creatorcontrib>Lai, Yen-Chang Clark</creatorcontrib><creatorcontrib>Lai, Yih-Shyong</creatorcontrib><creatorcontrib>Hsu, Yung-Hsiang</creatorcontrib><creatorcontrib>Liu, Yi-Hsiang</creatorcontrib><title>Plectin deficiency in liver cancer cells promotes cell migration and sensitivity to sorafenib treatment</title><title>Cell adhesion & migration</title><addtitle>Cell Adh Migr</addtitle><description>Plectin involved in activation of kinases in cell signaling pathway and plays important role in cell morphology and migration. Plectin knockdown promotes cell migration by activating focal adhesion kinase and Rac1-GTPase activity in liver cells. Sorafenib is a multi-targeting tyrosine kinase inhibitor that improves patient survival on hepatocellular carcinoma. The aim of this study is to investigate the correlation between the expression of plectin and cell migration as well as the sensitivity of hepatoma cell lines exposing to sorafenib. Hepatoma cell lines PLC/PRF/5 and HepG2 were used to examine the level of plectin expression and cell migration in comparison with Chang liver cell line. In addition, sensitivity of the 3 cell lines to sorafenib treatment was also measured. Expression of plectin was lower in PLC/PRF/5 and HepG2 hepatoma cells than that of Chang liver cells whereas HepG2 and PLC/PRF/5 cells exhibit higher rate of cell migration in trans-well migration assay. Immunohistofluorecent staining on E-cadherin revealed the highest rate of collective cell migration in HepG2 cells and the lowest was found in Chang liver cells. Likewise, HepG2 cell line was most sensitive to sorafenib treatment and Chang liver cells exhibited the least sensitivity. The drug sensitivity to sorafenib treatment showed inverse correlation with the expression of plectin. We suggest that plectin deficiency and increased E-cadherin in hepatoma cells were associated with higher rates of cell motility, collective cell migration as well as higher drug sensitivity to sorafenib treatment.</description><subject>Antineoplastic Agents - therapeutic use</subject><subject>Apoptosis - drug effects</subject><subject>Carcinoma, Hepatocellular - drug therapy</subject><subject>Carcinoma, Hepatocellular - metabolism</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement - drug effects</subject><subject>Cell Proliferation - drug effects</subject><subject>Cell Survival - drug effects</subject><subject>collective cell migration</subject><subject>cytoskeleton</subject><subject>E-cadherin</subject><subject>Hep G2 Cells</subject><subject>hepatocellular carcinoma</subject><subject>Humans</subject><subject>Liver Neoplasms - drug therapy</subject><subject>Liver Neoplasms - metabolism</subject><subject>Liver Neoplasms - pathology</subject><subject>plectin</subject><subject>Plectin - deficiency</subject><subject>Protein Kinase Inhibitors - pharmacology</subject><subject>Research Paper</subject><subject>Signal Transduction - drug effects</subject><subject>sorafenib</subject><subject>Sorafenib - pharmacology</subject><issn>1933-6918</issn><issn>1933-6926</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>0YH</sourceid><sourceid>EIF</sourceid><recordid>eNp9UUuP0zAQthCIXRZ-AshHLi0eJ3EmFwRa8ZJWggOcLdcZF6PELrZb1H-PQ7sVXDiNx_M9xv4Yew5iDQLFKxiaRg2AaymgX4NE7HF4wK6X-5UapHp4OQNesSc5_xCiQ1DqMbuSKPuKwWu2_TKRLT7wkZy3noI98tpN_kCJWxPsUmiaMt-lOMdC-U_LZ79NpvgYuAkjzxSyL_7gy5GXyHNMxlHwG14SmTJTKE_ZI2emTM_O9YZ9e__u6-3H1d3nD59u396tbKuwrBwAuRZtZ3sle6Sul5sOZJ0BIDaGpKMeRbvsr1RD1KkRW6qsFuxgqblhr0-6u_1mptFW62QmvUt-Numoo_H630nw3_U2HnT9GtEJWQVengVS_LmnXPTs8_JkEyjuswbsVTsoAapCuxPUpphzInexAaGXkPR9SHoJSZ9DqrwXf-94Yd2nUgFvTgAfXEyz-RXTNOpijlNMLtVQfNbN_z1-A7W1o64</recordid><startdate>20180102</startdate><enddate>20180102</enddate><creator>Cheng, Chiung-Chi</creator><creator>Chao, Wei-Ting</creator><creator>Liao, Chen-Chun</creator><creator>Tseng, Yu-Hui</creator><creator>Lai, Yen-Chang Clark</creator><creator>Lai, Yih-Shyong</creator><creator>Hsu, Yung-Hsiang</creator><creator>Liu, Yi-Hsiang</creator><general>Taylor & Francis</general><scope>0YH</scope><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>20180102</creationdate><title>Plectin deficiency in liver cancer cells promotes cell migration and sensitivity to sorafenib treatment</title><author>Cheng, Chiung-Chi ; Chao, Wei-Ting ; Liao, Chen-Chun ; Tseng, Yu-Hui ; Lai, Yen-Chang Clark ; Lai, Yih-Shyong ; Hsu, Yung-Hsiang ; Liu, Yi-Hsiang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c468t-f11ef48c5c76278e572b51246811883ae2fe78048276663ee56d84e11e41c9ce3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Antineoplastic Agents - therapeutic use</topic><topic>Apoptosis - drug effects</topic><topic>Carcinoma, Hepatocellular - drug therapy</topic><topic>Carcinoma, Hepatocellular - metabolism</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement - drug effects</topic><topic>Cell Proliferation - drug effects</topic><topic>Cell Survival - drug effects</topic><topic>collective cell migration</topic><topic>cytoskeleton</topic><topic>E-cadherin</topic><topic>Hep G2 Cells</topic><topic>hepatocellular carcinoma</topic><topic>Humans</topic><topic>Liver Neoplasms - drug therapy</topic><topic>Liver Neoplasms - metabolism</topic><topic>Liver Neoplasms - pathology</topic><topic>plectin</topic><topic>Plectin - deficiency</topic><topic>Protein Kinase Inhibitors - pharmacology</topic><topic>Research Paper</topic><topic>Signal Transduction - drug effects</topic><topic>sorafenib</topic><topic>Sorafenib - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cheng, Chiung-Chi</creatorcontrib><creatorcontrib>Chao, Wei-Ting</creatorcontrib><creatorcontrib>Liao, Chen-Chun</creatorcontrib><creatorcontrib>Tseng, Yu-Hui</creatorcontrib><creatorcontrib>Lai, Yen-Chang Clark</creatorcontrib><creatorcontrib>Lai, Yih-Shyong</creatorcontrib><creatorcontrib>Hsu, Yung-Hsiang</creatorcontrib><creatorcontrib>Liu, Yi-Hsiang</creatorcontrib><collection>Taylor & Francis Open Access</collection><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>Cell adhesion & migration</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cheng, Chiung-Chi</au><au>Chao, Wei-Ting</au><au>Liao, Chen-Chun</au><au>Tseng, Yu-Hui</au><au>Lai, Yen-Chang Clark</au><au>Lai, Yih-Shyong</au><au>Hsu, Yung-Hsiang</au><au>Liu, Yi-Hsiang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Plectin deficiency in liver cancer cells promotes cell migration and sensitivity to sorafenib treatment</atitle><jtitle>Cell adhesion & migration</jtitle><addtitle>Cell Adh Migr</addtitle><date>2018-01-02</date><risdate>2018</risdate><volume>12</volume><issue>1</issue><spage>19</spage><epage>27</epage><pages>19-27</pages><issn>1933-6918</issn><eissn>1933-6926</eissn><abstract>Plectin involved in activation of kinases in cell signaling pathway and plays important role in cell morphology and migration. Plectin knockdown promotes cell migration by activating focal adhesion kinase and Rac1-GTPase activity in liver cells. Sorafenib is a multi-targeting tyrosine kinase inhibitor that improves patient survival on hepatocellular carcinoma. The aim of this study is to investigate the correlation between the expression of plectin and cell migration as well as the sensitivity of hepatoma cell lines exposing to sorafenib. Hepatoma cell lines PLC/PRF/5 and HepG2 were used to examine the level of plectin expression and cell migration in comparison with Chang liver cell line. In addition, sensitivity of the 3 cell lines to sorafenib treatment was also measured. Expression of plectin was lower in PLC/PRF/5 and HepG2 hepatoma cells than that of Chang liver cells whereas HepG2 and PLC/PRF/5 cells exhibit higher rate of cell migration in trans-well migration assay. Immunohistofluorecent staining on E-cadherin revealed the highest rate of collective cell migration in HepG2 cells and the lowest was found in Chang liver cells. Likewise, HepG2 cell line was most sensitive to sorafenib treatment and Chang liver cells exhibited the least sensitivity. The drug sensitivity to sorafenib treatment showed inverse correlation with the expression of plectin. We suggest that plectin deficiency and increased E-cadherin in hepatoma cells were associated with higher rates of cell motility, collective cell migration as well as higher drug sensitivity to sorafenib treatment.</abstract><cop>United States</cop><pub>Taylor & Francis</pub><pmid>28276928</pmid><doi>10.1080/19336918.2017.1288789</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Antineoplastic Agents - therapeutic use Apoptosis - drug effects Carcinoma, Hepatocellular - drug therapy Carcinoma, Hepatocellular - metabolism Cell Line, Tumor Cell Movement - drug effects Cell Proliferation - drug effects Cell Survival - drug effects collective cell migration cytoskeleton E-cadherin Hep G2 Cells hepatocellular carcinoma Humans Liver Neoplasms - drug therapy Liver Neoplasms - metabolism Liver Neoplasms - pathology plectin Plectin - deficiency Protein Kinase Inhibitors - pharmacology Research Paper Signal Transduction - drug effects sorafenib Sorafenib - pharmacology |
| title | Plectin deficiency in liver cancer cells promotes cell migration and sensitivity to sorafenib treatment |
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