JWA regulates human esophageal squamous cell carcinoma and human esophageal cells through different mitogen-activated protein kinase signaling pathways
The aim of the present study was to investigate whether the JWA gene regulates the proliferation, migration and invasion of human esophageal squamous cell carcinoma (ESCC) and normal human esophageal cell lines through mitogen-activated protein kinase (MAPK) signal transduction pathways. The role of...
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creator | LIN, JIE MA, TIELIANG JIANG, XIAODONG GE, ZHIJUN DING, WEILIANG WU, YUANYUAN JIANG, GUOJUN FENG, JIAKE CUI, GUOXING TAN, YONGFEI |
description | The aim of the present study was to investigate whether the JWA gene regulates the proliferation, migration and invasion of human esophageal squamous cell carcinoma (ESCC) and normal human esophageal cell lines through mitogen-activated protein kinase (MAPK) signal transduction pathways. The role of JWA in proliferation, migration, invasion and apoptosis was investigated in the Eca109 human ESCC and HET-1A normal human esophageal cell lines via transfection with JWA-small interfering (si)RNA. Western blot analysis was conducted to observe the effect of JWA on apoptosis and the regulatory effect of JWA on proliferation was determined using a thiazolyl blue tetrazolium bromide (MTT) assay. Cellular migration and invasion were analyzed via a Transwell assay. In addition, the expression levels of extracellular signal-regulated protein kinases 1 and 2 (ERK1/2), c-Jun N-terminal kinase (JNK) and p38 MAPK following JWA-siRNA transfection were detected by western blot analysis and compared with those of untreated cells. The downregulation of JWA protein decreased apoptosis and increased the proliferation, migration and invasion of the Eca109 and HET-1A cell lines. In the Eca109 cell line, the expression levels of phosphorylated (p)-ERK1/2 and p-JNK, but not those of p-p38, decreased significantly in the JWA siRNA group compared with those in the control groups. However, in the HET-1A cell line, JWA-siRNA transfection significantly inhibited the expression of p-p38 and demonstrated no effect on the expression levels of p-ERK1/2 and p-JNK. In conclusion, the JWA gene may regulate the ESCC and human esophageal cell lines through MAPK signaling pathways via different regulatory mechanisms. |
doi_str_mv | 10.3892/etm.2014.1650 |
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The role of JWA in proliferation, migration, invasion and apoptosis was investigated in the Eca109 human ESCC and HET-1A normal human esophageal cell lines via transfection with JWA-small interfering (si)RNA. Western blot analysis was conducted to observe the effect of JWA on apoptosis and the regulatory effect of JWA on proliferation was determined using a thiazolyl blue tetrazolium bromide (MTT) assay. Cellular migration and invasion were analyzed via a Transwell assay. In addition, the expression levels of extracellular signal-regulated protein kinases 1 and 2 (ERK1/2), c-Jun N-terminal kinase (JNK) and p38 MAPK following JWA-siRNA transfection were detected by western blot analysis and compared with those of untreated cells. The downregulation of JWA protein decreased apoptosis and increased the proliferation, migration and invasion of the Eca109 and HET-1A cell lines. In the Eca109 cell line, the expression levels of phosphorylated (p)-ERK1/2 and p-JNK, but not those of p-p38, decreased significantly in the JWA siRNA group compared with those in the control groups. However, in the HET-1A cell line, JWA-siRNA transfection significantly inhibited the expression of p-p38 and demonstrated no effect on the expression levels of p-ERK1/2 and p-JNK. In conclusion, the JWA gene may regulate the ESCC and human esophageal cell lines through MAPK signaling pathways via different regulatory mechanisms.</description><identifier>ISSN: 1792-0981</identifier><identifier>EISSN: 1792-1015</identifier><identifier>DOI: 10.3892/etm.2014.1650</identifier><identifier>PMID: 24926382</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Analysis ; Antibiotics ; Apoptosis ; Care and treatment ; Cell adhesion & migration ; Cell cycle ; Cell growth ; Cellular signal transduction ; Control ; Esophageal cancer ; human esophageal cancer ; Immunoglobulins ; JWA ; Kinases ; Membranes ; Metabolism ; mitogen-activated protein kinase signaling pathway ; Phosphorylation ; Protein kinases ; Proteins ; Signal transduction ; small interfering RNA ; Squamous cell carcinoma</subject><ispartof>Experimental and therapeutic medicine, 2014-06, Vol.7 (6), p.1767-1771</ispartof><rights>Copyright © 2014, Spandidos Publications</rights><rights>COPYRIGHT 2014 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2014</rights><rights>Copyright © 2014, Spandidos Publications 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c514t-45451a6fc7ed0acc0a7133bdc4b69e43630223788abdea4a6c6300c6e240f8713</citedby><cites>FETCH-LOGICAL-c514t-45451a6fc7ed0acc0a7133bdc4b69e43630223788abdea4a6c6300c6e240f8713</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/PMC4043574/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4043574/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,886,27929,27930,53796,53798</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24926382$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>LIN, JIE</creatorcontrib><creatorcontrib>MA, TIELIANG</creatorcontrib><creatorcontrib>JIANG, XIAODONG</creatorcontrib><creatorcontrib>GE, ZHIJUN</creatorcontrib><creatorcontrib>DING, WEILIANG</creatorcontrib><creatorcontrib>WU, YUANYUAN</creatorcontrib><creatorcontrib>JIANG, GUOJUN</creatorcontrib><creatorcontrib>FENG, JIAKE</creatorcontrib><creatorcontrib>CUI, GUOXING</creatorcontrib><creatorcontrib>TAN, YONGFEI</creatorcontrib><title>JWA regulates human esophageal squamous cell carcinoma and human esophageal cells through different mitogen-activated protein kinase signaling pathways</title><title>Experimental and therapeutic medicine</title><addtitle>Exp Ther Med</addtitle><description>The aim of the present study was to investigate whether the JWA gene regulates the proliferation, migration and invasion of human esophageal squamous cell carcinoma (ESCC) and normal human esophageal cell lines through mitogen-activated protein kinase (MAPK) signal transduction pathways. The role of JWA in proliferation, migration, invasion and apoptosis was investigated in the Eca109 human ESCC and HET-1A normal human esophageal cell lines via transfection with JWA-small interfering (si)RNA. Western blot analysis was conducted to observe the effect of JWA on apoptosis and the regulatory effect of JWA on proliferation was determined using a thiazolyl blue tetrazolium bromide (MTT) assay. Cellular migration and invasion were analyzed via a Transwell assay. In addition, the expression levels of extracellular signal-regulated protein kinases 1 and 2 (ERK1/2), c-Jun N-terminal kinase (JNK) and p38 MAPK following JWA-siRNA transfection were detected by western blot analysis and compared with those of untreated cells. The downregulation of JWA protein decreased apoptosis and increased the proliferation, migration and invasion of the Eca109 and HET-1A cell lines. In the Eca109 cell line, the expression levels of phosphorylated (p)-ERK1/2 and p-JNK, but not those of p-p38, decreased significantly in the JWA siRNA group compared with those in the control groups. However, in the HET-1A cell line, JWA-siRNA transfection significantly inhibited the expression of p-p38 and demonstrated no effect on the expression levels of p-ERK1/2 and p-JNK. In conclusion, the JWA gene may regulate the ESCC and human esophageal cell lines through MAPK signaling pathways via different regulatory mechanisms.</description><subject>Analysis</subject><subject>Antibiotics</subject><subject>Apoptosis</subject><subject>Care and treatment</subject><subject>Cell adhesion & migration</subject><subject>Cell cycle</subject><subject>Cell growth</subject><subject>Cellular signal transduction</subject><subject>Control</subject><subject>Esophageal cancer</subject><subject>human esophageal cancer</subject><subject>Immunoglobulins</subject><subject>JWA</subject><subject>Kinases</subject><subject>Membranes</subject><subject>Metabolism</subject><subject>mitogen-activated protein kinase signaling pathway</subject><subject>Phosphorylation</subject><subject>Protein kinases</subject><subject>Proteins</subject><subject>Signal transduction</subject><subject>small interfering RNA</subject><subject>Squamous cell carcinoma</subject><issn>1792-0981</issn><issn>1792-1015</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNptkk1v1DAQhiMEolXpkSuyxAEuWezYcZwL0qriU5W4gDhas84kcUns1E5a9Zfwd3HYZaGAfbA1fuYde_xm2VNGN1zVxSucx01BmdgwWdIH2Smr6iJnlJUPD3taK3aSncd4RdMoJVOqfJydFKIuJFfFafb949ctCdgtA8wYSb-M4AhGP_XQIQwkXi8w-iUSg8NADARjnR-BgGv-hVcmkrkPful60ti2xYBuJqOdfYcuBzPbm1SnIVPwM1pHvlkHEUm0nYPBuo5MMPe3cBefZI9aGCKeH9az7MvbN58v3ueXn959uNhe5qZkYs5FKUoGsjUVNhSMoVAxzneNETtZo-CS06LglVKwaxAESJMi1EgsBG1VYs-y13vdadmN2Jh03QCDnoIdIdxpD1bfP3G2152_0YIKXlYiCbw8CAR_vWCc9Wjj2ghwmPqmmSqkpIyXPKHP_0Kv_BLSwxNV8_XbSlX_pjoYUFvX-lTXrKJ6K6iqFBc_qc1_qDQbHK3xDlub4vcS8n2CCT7GgO3xjYzq1Uw6mUmvZtKrmRL_7M_GHOlf1knAiz0Qp2QG2_h4ZJJSTqucypxVsuI_ALJm1NY</recordid><startdate>20140601</startdate><enddate>20140601</enddate><creator>LIN, JIE</creator><creator>MA, TIELIANG</creator><creator>JIANG, XIAODONG</creator><creator>GE, ZHIJUN</creator><creator>DING, WEILIANG</creator><creator>WU, YUANYUAN</creator><creator>JIANG, GUOJUN</creator><creator>FENG, JIAKE</creator><creator>CUI, GUOXING</creator><creator>TAN, YONGFEI</creator><general>D.A. Spandidos</general><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20140601</creationdate><title>JWA regulates human esophageal squamous cell carcinoma and human esophageal cells through different mitogen-activated protein kinase signaling pathways</title><author>LIN, JIE ; MA, TIELIANG ; JIANG, XIAODONG ; GE, ZHIJUN ; DING, WEILIANG ; WU, YUANYUAN ; JIANG, GUOJUN ; FENG, JIAKE ; CUI, GUOXING ; TAN, YONGFEI</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c514t-45451a6fc7ed0acc0a7133bdc4b69e43630223788abdea4a6c6300c6e240f8713</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Analysis</topic><topic>Antibiotics</topic><topic>Apoptosis</topic><topic>Care and treatment</topic><topic>Cell adhesion & migration</topic><topic>Cell cycle</topic><topic>Cell growth</topic><topic>Cellular signal transduction</topic><topic>Control</topic><topic>Esophageal cancer</topic><topic>human esophageal cancer</topic><topic>Immunoglobulins</topic><topic>JWA</topic><topic>Kinases</topic><topic>Membranes</topic><topic>Metabolism</topic><topic>mitogen-activated protein kinase signaling pathway</topic><topic>Phosphorylation</topic><topic>Protein kinases</topic><topic>Proteins</topic><topic>Signal transduction</topic><topic>small interfering RNA</topic><topic>Squamous cell carcinoma</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>LIN, JIE</creatorcontrib><creatorcontrib>MA, TIELIANG</creatorcontrib><creatorcontrib>JIANG, XIAODONG</creatorcontrib><creatorcontrib>GE, ZHIJUN</creatorcontrib><creatorcontrib>DING, WEILIANG</creatorcontrib><creatorcontrib>WU, YUANYUAN</creatorcontrib><creatorcontrib>JIANG, GUOJUN</creatorcontrib><creatorcontrib>FENG, JIAKE</creatorcontrib><creatorcontrib>CUI, GUOXING</creatorcontrib><creatorcontrib>TAN, YONGFEI</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Nursing & Allied Health Premium</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Experimental and therapeutic medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>LIN, JIE</au><au>MA, TIELIANG</au><au>JIANG, XIAODONG</au><au>GE, ZHIJUN</au><au>DING, WEILIANG</au><au>WU, YUANYUAN</au><au>JIANG, GUOJUN</au><au>FENG, JIAKE</au><au>CUI, GUOXING</au><au>TAN, YONGFEI</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>JWA regulates human esophageal squamous cell carcinoma and human esophageal cells through different mitogen-activated protein kinase signaling pathways</atitle><jtitle>Experimental and therapeutic medicine</jtitle><addtitle>Exp Ther Med</addtitle><date>2014-06-01</date><risdate>2014</risdate><volume>7</volume><issue>6</issue><spage>1767</spage><epage>1771</epage><pages>1767-1771</pages><issn>1792-0981</issn><eissn>1792-1015</eissn><abstract>The aim of the present study was to investigate whether the JWA gene regulates the proliferation, migration and invasion of human esophageal squamous cell carcinoma (ESCC) and normal human esophageal cell lines through mitogen-activated protein kinase (MAPK) signal transduction pathways. The role of JWA in proliferation, migration, invasion and apoptosis was investigated in the Eca109 human ESCC and HET-1A normal human esophageal cell lines via transfection with JWA-small interfering (si)RNA. Western blot analysis was conducted to observe the effect of JWA on apoptosis and the regulatory effect of JWA on proliferation was determined using a thiazolyl blue tetrazolium bromide (MTT) assay. Cellular migration and invasion were analyzed via a Transwell assay. In addition, the expression levels of extracellular signal-regulated protein kinases 1 and 2 (ERK1/2), c-Jun N-terminal kinase (JNK) and p38 MAPK following JWA-siRNA transfection were detected by western blot analysis and compared with those of untreated cells. The downregulation of JWA protein decreased apoptosis and increased the proliferation, migration and invasion of the Eca109 and HET-1A cell lines. In the Eca109 cell line, the expression levels of phosphorylated (p)-ERK1/2 and p-JNK, but not those of p-p38, decreased significantly in the JWA siRNA group compared with those in the control groups. However, in the HET-1A cell line, JWA-siRNA transfection significantly inhibited the expression of p-p38 and demonstrated no effect on the expression levels of p-ERK1/2 and p-JNK. In conclusion, the JWA gene may regulate the ESCC and human esophageal cell lines through MAPK signaling pathways via different regulatory mechanisms.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>24926382</pmid><doi>10.3892/etm.2014.1650</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Analysis Antibiotics Apoptosis Care and treatment Cell adhesion & migration Cell cycle Cell growth Cellular signal transduction Control Esophageal cancer human esophageal cancer Immunoglobulins JWA Kinases Membranes Metabolism mitogen-activated protein kinase signaling pathway Phosphorylation Protein kinases Proteins Signal transduction small interfering RNA Squamous cell carcinoma |
title | JWA regulates human esophageal squamous cell carcinoma and human esophageal cells through different mitogen-activated protein kinase signaling pathways |
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