Down-regulation of Gab1 inhibits cell proliferation and migration in hilar cholangiocarcinoma
Hilar cholangiocarcinoma is a highly aggressive malignancy originating from the hilar biliary duct epithelium. Due to few effective comprehensive treatments, the prognosis of hilar cholangiocarcinoma is poor. In this study, immunohistochemistry was first used to detect and analyze the expression of...
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| description | Hilar cholangiocarcinoma is a highly aggressive malignancy originating from the hilar biliary duct epithelium. Due to few effective comprehensive treatments, the prognosis of hilar cholangiocarcinoma is poor. In this study, immunohistochemistry was first used to detect and analyze the expression of Gab1, VEGFR-2, and MMP-9 in hilar cholangiocarcinoma solid tumors and the relationships to the clinical pathological features. Furthermore, Gab1 and VEGFR-2 siRNA were used to interfere the hilar cholangiocarcinoma cell line ICBD-1 and then detect the PI3K/Akt signaling pathway, MMP-9 levels and malignant biological behaviors of tumor cells. The data showed that 1. Gab1, VEGFR-2, and MMP-9 were highly expressed and positively correlated with each other in hilar cholangiocarcinoma tissues, which were related to lymph node metastasis and differentiation. 2. After Gab1 or VEGFR-2 siRNA interference, PI3K/Akt pathway activity and MMP-9 levels were decreased in ICBD-1 cells. At the same time, cell proliferation decreased, cell cycle arrested in G1 phase, apoptosis increased and invasion decreased. These results suggest that the expression of Gab1, VEGFR-2, and MMP-9 are significantly related to the malignant biological behavior of hilar cholangiocarcinoma. Gab1 regulates growth, apoptosis and invasion through the VEGFR-2/Gab1/PI3K/Akt signaling pathway in hilar cholangiocarcinoma cells and influences the invasion of tumor cells via MMP-9. |
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Due to few effective comprehensive treatments, the prognosis of hilar cholangiocarcinoma is poor. In this study, immunohistochemistry was first used to detect and analyze the expression of Gab1, VEGFR-2, and MMP-9 in hilar cholangiocarcinoma solid tumors and the relationships to the clinical pathological features. Furthermore, Gab1 and VEGFR-2 siRNA were used to interfere the hilar cholangiocarcinoma cell line ICBD-1 and then detect the PI3K/Akt signaling pathway, MMP-9 levels and malignant biological behaviors of tumor cells. The data showed that 1. Gab1, VEGFR-2, and MMP-9 were highly expressed and positively correlated with each other in hilar cholangiocarcinoma tissues, which were related to lymph node metastasis and differentiation. 2. After Gab1 or VEGFR-2 siRNA interference, PI3K/Akt pathway activity and MMP-9 levels were decreased in ICBD-1 cells. At the same time, cell proliferation decreased, cell cycle arrested in G1 phase, apoptosis increased and invasion decreased. These results suggest that the expression of Gab1, VEGFR-2, and MMP-9 are significantly related to the malignant biological behavior of hilar cholangiocarcinoma. Gab1 regulates growth, apoptosis and invasion through the VEGFR-2/Gab1/PI3K/Akt signaling pathway in hilar cholangiocarcinoma cells and influences the invasion of tumor cells via MMP-9.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0081347</identifier><identifier>PMID: 24312291</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>1-Phosphatidylinositol 3-kinase ; Adaptor Proteins, Signal Transducing - deficiency ; Adaptor Proteins, Signal Transducing - genetics ; Adaptor Proteins, Signal Transducing - metabolism ; AKT protein ; Apoptosis ; Bile Duct Neoplasms - genetics ; Bile Duct Neoplasms - pathology ; Bile Ducts, Intrahepatic - pathology ; Cancer ; Cell cycle ; Cell growth ; Cell Line, Tumor ; Cell migration ; Cell Movement - genetics ; Cell Proliferation ; Chemotherapy ; Cholangiocarcinoma ; Cholangiocarcinoma - genetics ; Cholangiocarcinoma - pathology ; Down-Regulation - genetics ; Epithelium ; G1 phase ; G1 Phase Cell Cycle Checkpoints - genetics ; Gelatinase B ; Gene Expression Regulation, Neoplastic ; Growth factors ; Hospitals ; Humans ; Immunohistochemistry ; Kinases ; Lymph nodes ; Malignancy ; Mammals ; Matrix Metalloproteinase 9 - genetics ; Matrix Metalloproteinase 9 - metabolism ; Medical prognosis ; Metastases ; Metastasis ; Phosphatidylinositol 3-Kinases - metabolism ; Proto-Oncogene Proteins c-akt - metabolism ; Radiation therapy ; RNA Interference ; RNA, Small Interfering - genetics ; Signal transduction ; Signal Transduction - genetics ; Signaling ; siRNA ; Solid tumors ; Surgery ; Tissues ; Tumor cells ; Tumors ; Vascular Endothelial Growth Factor Receptor-2 - deficiency ; Vascular Endothelial Growth Factor Receptor-2 - genetics ; Vascular Endothelial Growth Factor Receptor-2 - metabolism ; Vascular endothelial growth factor receptors</subject><ispartof>PloS one, 2013-11, Vol.8 (11), p.e81347-e81347</ispartof><rights>2013 Sang et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/3.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2013 Sang et al 2013 Sang et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c592t-3784102a5dcb706f41979e3c4893f7519410160f8c085e48ed9db421b24e7f7a3</citedby><cites>FETCH-LOGICAL-c592t-3784102a5dcb706f41979e3c4893f7519410160f8c085e48ed9db421b24e7f7a3</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/PMC3842939/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3842939/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793,79600,79601</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24312291$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Bunting, Kevin D</contributor><creatorcontrib>Sang, Haiquan</creatorcontrib><creatorcontrib>Li, Tingting</creatorcontrib><creatorcontrib>Li, Hangyu</creatorcontrib><creatorcontrib>Liu, Jingang</creatorcontrib><title>Down-regulation of Gab1 inhibits cell proliferation and migration in hilar cholangiocarcinoma</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Hilar cholangiocarcinoma is a highly aggressive malignancy originating from the hilar biliary duct epithelium. Due to few effective comprehensive treatments, the prognosis of hilar cholangiocarcinoma is poor. In this study, immunohistochemistry was first used to detect and analyze the expression of Gab1, VEGFR-2, and MMP-9 in hilar cholangiocarcinoma solid tumors and the relationships to the clinical pathological features. Furthermore, Gab1 and VEGFR-2 siRNA were used to interfere the hilar cholangiocarcinoma cell line ICBD-1 and then detect the PI3K/Akt signaling pathway, MMP-9 levels and malignant biological behaviors of tumor cells. The data showed that 1. Gab1, VEGFR-2, and MMP-9 were highly expressed and positively correlated with each other in hilar cholangiocarcinoma tissues, which were related to lymph node metastasis and differentiation. 2. After Gab1 or VEGFR-2 siRNA interference, PI3K/Akt pathway activity and MMP-9 levels were decreased in ICBD-1 cells. At the same time, cell proliferation decreased, cell cycle arrested in G1 phase, apoptosis increased and invasion decreased. These results suggest that the expression of Gab1, VEGFR-2, and MMP-9 are significantly related to the malignant biological behavior of hilar cholangiocarcinoma. Gab1 regulates growth, apoptosis and invasion through the VEGFR-2/Gab1/PI3K/Akt signaling pathway in hilar cholangiocarcinoma cells and influences the invasion of tumor cells via MMP-9.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>Adaptor Proteins, Signal Transducing - deficiency</subject><subject>Adaptor Proteins, Signal Transducing - genetics</subject><subject>Adaptor Proteins, Signal Transducing - metabolism</subject><subject>AKT protein</subject><subject>Apoptosis</subject><subject>Bile Duct Neoplasms - genetics</subject><subject>Bile Duct Neoplasms - pathology</subject><subject>Bile Ducts, Intrahepatic - pathology</subject><subject>Cancer</subject><subject>Cell cycle</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell migration</subject><subject>Cell Movement - genetics</subject><subject>Cell Proliferation</subject><subject>Chemotherapy</subject><subject>Cholangiocarcinoma</subject><subject>Cholangiocarcinoma - genetics</subject><subject>Cholangiocarcinoma - pathology</subject><subject>Down-Regulation - genetics</subject><subject>Epithelium</subject><subject>G1 phase</subject><subject>G1 Phase Cell Cycle Checkpoints - genetics</subject><subject>Gelatinase B</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Growth factors</subject><subject>Hospitals</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Kinases</subject><subject>Lymph nodes</subject><subject>Malignancy</subject><subject>Mammals</subject><subject>Matrix Metalloproteinase 9 - genetics</subject><subject>Matrix Metalloproteinase 9 - metabolism</subject><subject>Medical prognosis</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Radiation therapy</subject><subject>RNA Interference</subject><subject>RNA, Small Interfering - genetics</subject><subject>Signal transduction</subject><subject>Signal Transduction - genetics</subject><subject>Signaling</subject><subject>siRNA</subject><subject>Solid tumors</subject><subject>Surgery</subject><subject>Tissues</subject><subject>Tumor cells</subject><subject>Tumors</subject><subject>Vascular Endothelial Growth Factor Receptor-2 - deficiency</subject><subject>Vascular Endothelial Growth Factor Receptor-2 - genetics</subject><subject>Vascular Endothelial Growth Factor Receptor-2 - metabolism</subject><subject>Vascular endothelial growth factor receptors</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNptUk1v1DAUtBCIlsI_QBCJC5csfrbjjwsSKlAqVeICR2Q5jpP1yrEXOwH13zfbTasWcfLHm5k372kQeg14A1TAh12aczRhs0_RbTCWQJl4gk5BUVJzgunTB_cT9KKUHcYNlZw_RyeEUSBEwSn69Tn9jXV2wxzM5FOsUl9dmBYqH7e-9VOprAuh2ucUfO_yEWNiV41-WF8-VlsfTK7sNgUTB5-sydbHNJqX6FlvQnGv1vMM_fz65cf5t_rq-8Xl-aer2jaKTDUVkgEmpulsKzDvGSihHLVMKtqLBtRSBY57abFsHJOuU13LCLSEOdELQ8_Q26PuPqSi180UDYwTJjhp2IK4PCK6ZHZ6n_1o8rVOxuvbj5QHbfLkbXCaAlPQcow55gw6KZfWGOziy3DSMrlofVy7ze3oOuvilE14JPq4Ev1WD-mPppIRRdUi8H4VyOn37MqkR18OezbRpfnWdyM5EIkX6Lt_oP-fjh1RNqdSsuvvzQDWh7TcsfQhLXpNy0J783CQe9JdPOgNREu8Yw</recordid><startdate>20131128</startdate><enddate>20131128</enddate><creator>Sang, Haiquan</creator><creator>Li, Tingting</creator><creator>Li, Hangyu</creator><creator>Liu, Jingang</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20131128</creationdate><title>Down-regulation of Gab1 inhibits cell proliferation and migration in hilar cholangiocarcinoma</title><author>Sang, Haiquan ; Li, Tingting ; Li, Hangyu ; Liu, Jingang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c592t-3784102a5dcb706f41979e3c4893f7519410160f8c085e48ed9db421b24e7f7a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>Adaptor Proteins, Signal Transducing - deficiency</topic><topic>Adaptor Proteins, Signal Transducing - genetics</topic><topic>Adaptor Proteins, Signal Transducing - metabolism</topic><topic>AKT protein</topic><topic>Apoptosis</topic><topic>Bile Duct Neoplasms - genetics</topic><topic>Bile Duct Neoplasms - pathology</topic><topic>Bile Ducts, Intrahepatic - pathology</topic><topic>Cancer</topic><topic>Cell cycle</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell migration</topic><topic>Cell Movement - genetics</topic><topic>Cell Proliferation</topic><topic>Chemotherapy</topic><topic>Cholangiocarcinoma</topic><topic>Cholangiocarcinoma - genetics</topic><topic>Cholangiocarcinoma - pathology</topic><topic>Down-Regulation - genetics</topic><topic>Epithelium</topic><topic>G1 phase</topic><topic>G1 Phase Cell Cycle Checkpoints - genetics</topic><topic>Gelatinase B</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Growth factors</topic><topic>Hospitals</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Kinases</topic><topic>Lymph nodes</topic><topic>Malignancy</topic><topic>Mammals</topic><topic>Matrix Metalloproteinase 9 - genetics</topic><topic>Matrix Metalloproteinase 9 - metabolism</topic><topic>Medical prognosis</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Radiation therapy</topic><topic>RNA Interference</topic><topic>RNA, Small Interfering - genetics</topic><topic>Signal transduction</topic><topic>Signal Transduction - genetics</topic><topic>Signaling</topic><topic>siRNA</topic><topic>Solid tumors</topic><topic>Surgery</topic><topic>Tissues</topic><topic>Tumor cells</topic><topic>Tumors</topic><topic>Vascular Endothelial Growth Factor Receptor-2 - deficiency</topic><topic>Vascular Endothelial Growth Factor Receptor-2 - genetics</topic><topic>Vascular Endothelial Growth Factor Receptor-2 - metabolism</topic><topic>Vascular endothelial growth factor receptors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sang, Haiquan</creatorcontrib><creatorcontrib>Li, Tingting</creatorcontrib><creatorcontrib>Li, Hangyu</creatorcontrib><creatorcontrib>Liu, Jingang</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>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</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>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 & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</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>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sang, Haiquan</au><au>Li, Tingting</au><au>Li, Hangyu</au><au>Liu, Jingang</au><au>Bunting, Kevin D</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Down-regulation of Gab1 inhibits cell proliferation and migration in hilar cholangiocarcinoma</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2013-11-28</date><risdate>2013</risdate><volume>8</volume><issue>11</issue><spage>e81347</spage><epage>e81347</epage><pages>e81347-e81347</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Hilar cholangiocarcinoma is a highly aggressive malignancy originating from the hilar biliary duct epithelium. Due to few effective comprehensive treatments, the prognosis of hilar cholangiocarcinoma is poor. In this study, immunohistochemistry was first used to detect and analyze the expression of Gab1, VEGFR-2, and MMP-9 in hilar cholangiocarcinoma solid tumors and the relationships to the clinical pathological features. Furthermore, Gab1 and VEGFR-2 siRNA were used to interfere the hilar cholangiocarcinoma cell line ICBD-1 and then detect the PI3K/Akt signaling pathway, MMP-9 levels and malignant biological behaviors of tumor cells. The data showed that 1. Gab1, VEGFR-2, and MMP-9 were highly expressed and positively correlated with each other in hilar cholangiocarcinoma tissues, which were related to lymph node metastasis and differentiation. 2. After Gab1 or VEGFR-2 siRNA interference, PI3K/Akt pathway activity and MMP-9 levels were decreased in ICBD-1 cells. At the same time, cell proliferation decreased, cell cycle arrested in G1 phase, apoptosis increased and invasion decreased. These results suggest that the expression of Gab1, VEGFR-2, and MMP-9 are significantly related to the malignant biological behavior of hilar cholangiocarcinoma. Gab1 regulates growth, apoptosis and invasion through the VEGFR-2/Gab1/PI3K/Akt signaling pathway in hilar cholangiocarcinoma cells and influences the invasion of tumor cells via MMP-9.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>24312291</pmid><doi>10.1371/journal.pone.0081347</doi><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 1932-6203 |
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| issn | 1932-6203 1932-6203 |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS); EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | 1-Phosphatidylinositol 3-kinase Adaptor Proteins, Signal Transducing - deficiency Adaptor Proteins, Signal Transducing - genetics Adaptor Proteins, Signal Transducing - metabolism AKT protein Apoptosis Bile Duct Neoplasms - genetics Bile Duct Neoplasms - pathology Bile Ducts, Intrahepatic - pathology Cancer Cell cycle Cell growth Cell Line, Tumor Cell migration Cell Movement - genetics Cell Proliferation Chemotherapy Cholangiocarcinoma Cholangiocarcinoma - genetics Cholangiocarcinoma - pathology Down-Regulation - genetics Epithelium G1 phase G1 Phase Cell Cycle Checkpoints - genetics Gelatinase B Gene Expression Regulation, Neoplastic Growth factors Hospitals Humans Immunohistochemistry Kinases Lymph nodes Malignancy Mammals Matrix Metalloproteinase 9 - genetics Matrix Metalloproteinase 9 - metabolism Medical prognosis Metastases Metastasis Phosphatidylinositol 3-Kinases - metabolism Proto-Oncogene Proteins c-akt - metabolism Radiation therapy RNA Interference RNA, Small Interfering - genetics Signal transduction Signal Transduction - genetics Signaling siRNA Solid tumors Surgery Tissues Tumor cells Tumors Vascular Endothelial Growth Factor Receptor-2 - deficiency Vascular Endothelial Growth Factor Receptor-2 - genetics Vascular Endothelial Growth Factor Receptor-2 - metabolism Vascular endothelial growth factor receptors |
| title | Down-regulation of Gab1 inhibits cell proliferation and migration in hilar cholangiocarcinoma |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-05T23%3A21%3A23IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Down-regulation%20of%20Gab1%20inhibits%20cell%20proliferation%20and%20migration%20in%20hilar%20cholangiocarcinoma&rft.jtitle=PloS%20one&rft.au=Sang,%20Haiquan&rft.date=2013-11-28&rft.volume=8&rft.issue=11&rft.spage=e81347&rft.epage=e81347&rft.pages=e81347-e81347&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0081347&rft_dat=%3Cproquest_plos_%3E3141001381%3C/proquest_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1462476254&rft_id=info:pmid/24312291&rft_doaj_id=oai_doaj_org_article_31491b60060641d8816001c06fa62b48&rfr_iscdi=true |