C1GALT1 promotes invasive phenotypes of hepatocellular carcinoma cells by modulating integrin β1 glycosylation and activity
Cancer cell invasion and metastasis are the primary causes of treatment failure and death in hepatocellular carcinoma (HCC). We previously reported that core 1 β1,3-galactosyltransferase (C1GALT1) is frequently overexpressed in HCC tumors and its expression is associated with advanced tumor stage, m...
Gespeichert in:
| Veröffentlicht in: | PloS one 2014-08, Vol.9 (8), p.e94995-e94995 |
|---|---|
| Hauptverfasser: | , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | e94995 |
|---|---|
| container_issue | 8 |
| container_start_page | e94995 |
| container_title | PloS one |
| container_volume | 9 |
| creator | Liu, Chiung-Hui Hu, Rey-Heng Huang, Miao-Juei Lai, I-Rue Chen, Chia-Hua Lai, Hong-Shiee Wu, Yao-Ming Huang, Min-Chuan |
| description | Cancer cell invasion and metastasis are the primary causes of treatment failure and death in hepatocellular carcinoma (HCC). We previously reported that core 1 β1,3-galactosyltransferase (C1GALT1) is frequently overexpressed in HCC tumors and its expression is associated with advanced tumor stage, metastasis, and poor survival. However, the underlying mechanisms of C1GALT1 in HCC malignancy remain unclear. In this study, we found that overexpression of C1GALT1 enhanced HCC cell adhesion to extracellular matrix (ECM) proteins, migration, and invasion, whereas RNAi-mediated knockdown of C1GALT1 suppressed these phenotypes. The promoting effect of C1GALT1 on the metastasis of HCC cells was demonstrated in a mouse xenograft model. Mechanistic investigations showed that the C1GALT1-enhanced phenotypic changes in HCC cells were significantly suppressed by anti-integrin β1 blocking antibody. Moreover, C1GALT1 was able to modify O-glycans on integrin β1 and regulate integrin β1 activity as well as its downstream signaling. These results suggest that C1GALT1 could enhance HCC invasiveness through integrin β1 and provide novel insights into the roles of O-glycosylation in HCC metastasis. |
| doi_str_mv | 10.1371/journal.pone.0094995 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_plos_</sourceid><recordid>TN_cdi_plos_journals_1551148454</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><doaj_id>oai_doaj_org_article_e413e7d74f5948ddbec85a24b2f1749f</doaj_id><sourcerecordid>1551608584</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4415-ce1813ae7e1453dea9c3f564387998e99f47cb62b2684f60da004c0a197a73c33</originalsourceid><addsrcrecordid>eNptUsFq3DAQNaWlSdP-QWkFvfSyW40l2dKlEJYkDSz0kp6FLI93tdiSK3kXDPmqfki_qXZ3E5LSk8S8N2_eDC_L3gNdAivhyy7sozftsg8el5QqrpR4kZ2DYvmiyCl7-eR_lr1JaUepYLIoXmdnuaBSiUKdZ_cruLlc3wHpY-jCgIk4fzDJHZD0W_RhGPupFhqyxd4MwWLb7lsTiTXROh86Q-ZSItVIulBP0OD8ZtIYcBOdJ79_Adm0ow1pnKHgifE1MXZwBzeMb7NXjWkTvju9F9mP66u71bfF-vvN7epyvbCcg1hYBAnMYInABavRKMsaUXAmS6UkKtXw0lZFXuWF5E1Ba0Mpt9SAKk3JLGMX2cejbt-GpE-HSxqEAOCSCz4xbo-MOpid7qPrTBx1ME7_LYS40SYOzraokQPDsi55IxSXdV2hlcLkvMobKLlqJq2vp2n7qsPaoh-iaZ-JPke82-pNOGgOOdASJoHPJ4EYfu4xDbpzaT6z8Rj2R98FlULOvj_9Q_3_dvzIsjGkFLF5NANUz2F66NJzmPQpTFPbh6eLPDY9pIf9AWzxytM</addsrcrecordid><sourcetype>Open Website</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1551148454</pqid></control><display><type>article</type><title>C1GALT1 promotes invasive phenotypes of hepatocellular carcinoma cells by modulating integrin β1 glycosylation and activity</title><source>MEDLINE</source><source>DOAJ Directory of Open Access Journals</source><source>Public Library of Science (PLoS) Journals Open Access</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><source>Free Full-Text Journals in Chemistry</source><creator>Liu, Chiung-Hui ; Hu, Rey-Heng ; Huang, Miao-Juei ; Lai, I-Rue ; Chen, Chia-Hua ; Lai, Hong-Shiee ; Wu, Yao-Ming ; Huang, Min-Chuan</creator><contributor>Papa, Salvatore</contributor><creatorcontrib>Liu, Chiung-Hui ; Hu, Rey-Heng ; Huang, Miao-Juei ; Lai, I-Rue ; Chen, Chia-Hua ; Lai, Hong-Shiee ; Wu, Yao-Ming ; Huang, Min-Chuan ; Papa, Salvatore</creatorcontrib><description>Cancer cell invasion and metastasis are the primary causes of treatment failure and death in hepatocellular carcinoma (HCC). We previously reported that core 1 β1,3-galactosyltransferase (C1GALT1) is frequently overexpressed in HCC tumors and its expression is associated with advanced tumor stage, metastasis, and poor survival. However, the underlying mechanisms of C1GALT1 in HCC malignancy remain unclear. In this study, we found that overexpression of C1GALT1 enhanced HCC cell adhesion to extracellular matrix (ECM) proteins, migration, and invasion, whereas RNAi-mediated knockdown of C1GALT1 suppressed these phenotypes. The promoting effect of C1GALT1 on the metastasis of HCC cells was demonstrated in a mouse xenograft model. Mechanistic investigations showed that the C1GALT1-enhanced phenotypic changes in HCC cells were significantly suppressed by anti-integrin β1 blocking antibody. Moreover, C1GALT1 was able to modify O-glycans on integrin β1 and regulate integrin β1 activity as well as its downstream signaling. These results suggest that C1GALT1 could enhance HCC invasiveness through integrin β1 and provide novel insights into the roles of O-glycosylation in HCC metastasis.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0094995</identifier><identifier>PMID: 25089569</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Animals ; Antibodies, Neutralizing - pharmacology ; Antigens ; Biology and Life Sciences ; Blocking antibodies ; Carcinoma, Hepatocellular - drug therapy ; Carcinoma, Hepatocellular - genetics ; Carcinoma, Hepatocellular - metabolism ; Carcinoma, Hepatocellular - secondary ; Cell adhesion ; Cell adhesion & migration ; Cell Adhesion - drug effects ; Cell cycle ; Cell growth ; Cell Line, Tumor ; Cell Movement - drug effects ; Cloning ; Developmental biology ; Experiments ; Extracellular matrix ; Extracellular Matrix Proteins - genetics ; Extracellular Matrix Proteins - metabolism ; Female ; Galactosyltransferases - antagonists & inhibitors ; Galactosyltransferases - genetics ; Galactosyltransferases - metabolism ; Gene expression ; Gene Expression Regulation, Neoplastic ; Glycosylation ; Hepatocellular carcinoma ; Hepatology ; Humans ; Immunoglobulins ; Integrin beta1 - genetics ; Integrin beta1 - metabolism ; Invasiveness ; Kinases ; Liver cancer ; Liver Neoplasms, Experimental - drug therapy ; Liver Neoplasms, Experimental - genetics ; Liver Neoplasms, Experimental - metabolism ; Liver Neoplasms, Experimental - pathology ; Lung Neoplasms - drug therapy ; Lung Neoplasms - genetics ; Lung Neoplasms - metabolism ; Lung Neoplasms - secondary ; Malignancy ; Medicine ; Medicine and Health Sciences ; Metastases ; Metastasis ; Mice ; Mice, SCID ; Neoplasm Invasiveness ; Physical Sciences ; Polysaccharides ; Polysaccharides - chemistry ; Polysaccharides - metabolism ; Protein Binding ; Proteins ; RNA, Small Interfering - genetics ; RNA, Small Interfering - metabolism ; RNA-mediated interference ; Signal Transduction ; Signaling ; Surgery ; Tumors ; Xenografts ; Xenotransplantation</subject><ispartof>PloS one, 2014-08, Vol.9 (8), p.e94995-e94995</ispartof><rights>2014 Liu et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (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>2014 Liu et al 2014 Liu et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4415-ce1813ae7e1453dea9c3f564387998e99f47cb62b2684f60da004c0a197a73c33</citedby><cites>FETCH-LOGICAL-c4415-ce1813ae7e1453dea9c3f564387998e99f47cb62b2684f60da004c0a197a73c33</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/PMC4121071/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4121071/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,865,886,2103,2929,23871,27929,27930,53796,53798</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25089569$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Papa, Salvatore</contributor><creatorcontrib>Liu, Chiung-Hui</creatorcontrib><creatorcontrib>Hu, Rey-Heng</creatorcontrib><creatorcontrib>Huang, Miao-Juei</creatorcontrib><creatorcontrib>Lai, I-Rue</creatorcontrib><creatorcontrib>Chen, Chia-Hua</creatorcontrib><creatorcontrib>Lai, Hong-Shiee</creatorcontrib><creatorcontrib>Wu, Yao-Ming</creatorcontrib><creatorcontrib>Huang, Min-Chuan</creatorcontrib><title>C1GALT1 promotes invasive phenotypes of hepatocellular carcinoma cells by modulating integrin β1 glycosylation and activity</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Cancer cell invasion and metastasis are the primary causes of treatment failure and death in hepatocellular carcinoma (HCC). We previously reported that core 1 β1,3-galactosyltransferase (C1GALT1) is frequently overexpressed in HCC tumors and its expression is associated with advanced tumor stage, metastasis, and poor survival. However, the underlying mechanisms of C1GALT1 in HCC malignancy remain unclear. In this study, we found that overexpression of C1GALT1 enhanced HCC cell adhesion to extracellular matrix (ECM) proteins, migration, and invasion, whereas RNAi-mediated knockdown of C1GALT1 suppressed these phenotypes. The promoting effect of C1GALT1 on the metastasis of HCC cells was demonstrated in a mouse xenograft model. Mechanistic investigations showed that the C1GALT1-enhanced phenotypic changes in HCC cells were significantly suppressed by anti-integrin β1 blocking antibody. Moreover, C1GALT1 was able to modify O-glycans on integrin β1 and regulate integrin β1 activity as well as its downstream signaling. These results suggest that C1GALT1 could enhance HCC invasiveness through integrin β1 and provide novel insights into the roles of O-glycosylation in HCC metastasis.</description><subject>Animals</subject><subject>Antibodies, Neutralizing - pharmacology</subject><subject>Antigens</subject><subject>Biology and Life Sciences</subject><subject>Blocking antibodies</subject><subject>Carcinoma, Hepatocellular - drug therapy</subject><subject>Carcinoma, Hepatocellular - genetics</subject><subject>Carcinoma, Hepatocellular - metabolism</subject><subject>Carcinoma, Hepatocellular - secondary</subject><subject>Cell adhesion</subject><subject>Cell adhesion & migration</subject><subject>Cell Adhesion - drug effects</subject><subject>Cell cycle</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement - drug effects</subject><subject>Cloning</subject><subject>Developmental biology</subject><subject>Experiments</subject><subject>Extracellular matrix</subject><subject>Extracellular Matrix Proteins - genetics</subject><subject>Extracellular Matrix Proteins - metabolism</subject><subject>Female</subject><subject>Galactosyltransferases - antagonists & inhibitors</subject><subject>Galactosyltransferases - genetics</subject><subject>Galactosyltransferases - metabolism</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Glycosylation</subject><subject>Hepatocellular carcinoma</subject><subject>Hepatology</subject><subject>Humans</subject><subject>Immunoglobulins</subject><subject>Integrin beta1 - genetics</subject><subject>Integrin beta1 - metabolism</subject><subject>Invasiveness</subject><subject>Kinases</subject><subject>Liver cancer</subject><subject>Liver Neoplasms, Experimental - drug therapy</subject><subject>Liver Neoplasms, Experimental - genetics</subject><subject>Liver Neoplasms, Experimental - metabolism</subject><subject>Liver Neoplasms, Experimental - pathology</subject><subject>Lung Neoplasms - drug therapy</subject><subject>Lung Neoplasms - genetics</subject><subject>Lung Neoplasms - metabolism</subject><subject>Lung Neoplasms - secondary</subject><subject>Malignancy</subject><subject>Medicine</subject><subject>Medicine and Health Sciences</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>Mice</subject><subject>Mice, SCID</subject><subject>Neoplasm Invasiveness</subject><subject>Physical Sciences</subject><subject>Polysaccharides</subject><subject>Polysaccharides - chemistry</subject><subject>Polysaccharides - metabolism</subject><subject>Protein Binding</subject><subject>Proteins</subject><subject>RNA, Small Interfering - genetics</subject><subject>RNA, Small Interfering - metabolism</subject><subject>RNA-mediated interference</subject><subject>Signal Transduction</subject><subject>Signaling</subject><subject>Surgery</subject><subject>Tumors</subject><subject>Xenografts</subject><subject>Xenotransplantation</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</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>eNptUsFq3DAQNaWlSdP-QWkFvfSyW40l2dKlEJYkDSz0kp6FLI93tdiSK3kXDPmqfki_qXZ3E5LSk8S8N2_eDC_L3gNdAivhyy7sozftsg8el5QqrpR4kZ2DYvmiyCl7-eR_lr1JaUepYLIoXmdnuaBSiUKdZ_cruLlc3wHpY-jCgIk4fzDJHZD0W_RhGPupFhqyxd4MwWLb7lsTiTXROh86Q-ZSItVIulBP0OD8ZtIYcBOdJ79_Adm0ow1pnKHgifE1MXZwBzeMb7NXjWkTvju9F9mP66u71bfF-vvN7epyvbCcg1hYBAnMYInABavRKMsaUXAmS6UkKtXw0lZFXuWF5E1Ba0Mpt9SAKk3JLGMX2cejbt-GpE-HSxqEAOCSCz4xbo-MOpid7qPrTBx1ME7_LYS40SYOzraokQPDsi55IxSXdV2hlcLkvMobKLlqJq2vp2n7qsPaoh-iaZ-JPke82-pNOGgOOdASJoHPJ4EYfu4xDbpzaT6z8Rj2R98FlULOvj_9Q_3_dvzIsjGkFLF5NANUz2F66NJzmPQpTFPbh6eLPDY9pIf9AWzxytM</recordid><startdate>20140804</startdate><enddate>20140804</enddate><creator>Liu, Chiung-Hui</creator><creator>Hu, Rey-Heng</creator><creator>Huang, Miao-Juei</creator><creator>Lai, I-Rue</creator><creator>Chen, Chia-Hua</creator><creator>Lai, Hong-Shiee</creator><creator>Wu, Yao-Ming</creator><creator>Huang, Min-Chuan</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>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20140804</creationdate><title>C1GALT1 promotes invasive phenotypes of hepatocellular carcinoma cells by modulating integrin β1 glycosylation and activity</title><author>Liu, Chiung-Hui ; Hu, Rey-Heng ; Huang, Miao-Juei ; Lai, I-Rue ; Chen, Chia-Hua ; Lai, Hong-Shiee ; Wu, Yao-Ming ; Huang, Min-Chuan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4415-ce1813ae7e1453dea9c3f564387998e99f47cb62b2684f60da004c0a197a73c33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Animals</topic><topic>Antibodies, Neutralizing - pharmacology</topic><topic>Antigens</topic><topic>Biology and Life Sciences</topic><topic>Blocking antibodies</topic><topic>Carcinoma, Hepatocellular - drug therapy</topic><topic>Carcinoma, Hepatocellular - genetics</topic><topic>Carcinoma, Hepatocellular - metabolism</topic><topic>Carcinoma, Hepatocellular - secondary</topic><topic>Cell adhesion</topic><topic>Cell adhesion & migration</topic><topic>Cell Adhesion - drug effects</topic><topic>Cell cycle</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement - drug effects</topic><topic>Cloning</topic><topic>Developmental biology</topic><topic>Experiments</topic><topic>Extracellular matrix</topic><topic>Extracellular Matrix Proteins - genetics</topic><topic>Extracellular Matrix Proteins - metabolism</topic><topic>Female</topic><topic>Galactosyltransferases - antagonists & inhibitors</topic><topic>Galactosyltransferases - genetics</topic><topic>Galactosyltransferases - metabolism</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Glycosylation</topic><topic>Hepatocellular carcinoma</topic><topic>Hepatology</topic><topic>Humans</topic><topic>Immunoglobulins</topic><topic>Integrin beta1 - genetics</topic><topic>Integrin beta1 - metabolism</topic><topic>Invasiveness</topic><topic>Kinases</topic><topic>Liver cancer</topic><topic>Liver Neoplasms, Experimental - drug therapy</topic><topic>Liver Neoplasms, Experimental - genetics</topic><topic>Liver Neoplasms, Experimental - metabolism</topic><topic>Liver Neoplasms, Experimental - pathology</topic><topic>Lung Neoplasms - drug therapy</topic><topic>Lung Neoplasms - genetics</topic><topic>Lung Neoplasms - metabolism</topic><topic>Lung Neoplasms - secondary</topic><topic>Malignancy</topic><topic>Medicine</topic><topic>Medicine and Health Sciences</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>Mice</topic><topic>Mice, SCID</topic><topic>Neoplasm Invasiveness</topic><topic>Physical Sciences</topic><topic>Polysaccharides</topic><topic>Polysaccharides - chemistry</topic><topic>Polysaccharides - metabolism</topic><topic>Protein Binding</topic><topic>Proteins</topic><topic>RNA, Small Interfering - genetics</topic><topic>RNA, Small Interfering - metabolism</topic><topic>RNA-mediated interference</topic><topic>Signal Transduction</topic><topic>Signaling</topic><topic>Surgery</topic><topic>Tumors</topic><topic>Xenografts</topic><topic>Xenotransplantation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Chiung-Hui</creatorcontrib><creatorcontrib>Hu, Rey-Heng</creatorcontrib><creatorcontrib>Huang, Miao-Juei</creatorcontrib><creatorcontrib>Lai, I-Rue</creatorcontrib><creatorcontrib>Chen, Chia-Hua</creatorcontrib><creatorcontrib>Lai, Hong-Shiee</creatorcontrib><creatorcontrib>Wu, Yao-Ming</creatorcontrib><creatorcontrib>Huang, Min-Chuan</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 - Academic</collection><collection>ProQuest Engineering Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Agricultural Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Engineering Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>Materials Science Collection</collection><collection>Access via ProQuest (Open Access)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - 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>Liu, Chiung-Hui</au><au>Hu, Rey-Heng</au><au>Huang, Miao-Juei</au><au>Lai, I-Rue</au><au>Chen, Chia-Hua</au><au>Lai, Hong-Shiee</au><au>Wu, Yao-Ming</au><au>Huang, Min-Chuan</au><au>Papa, Salvatore</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>C1GALT1 promotes invasive phenotypes of hepatocellular carcinoma cells by modulating integrin β1 glycosylation and activity</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2014-08-04</date><risdate>2014</risdate><volume>9</volume><issue>8</issue><spage>e94995</spage><epage>e94995</epage><pages>e94995-e94995</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Cancer cell invasion and metastasis are the primary causes of treatment failure and death in hepatocellular carcinoma (HCC). We previously reported that core 1 β1,3-galactosyltransferase (C1GALT1) is frequently overexpressed in HCC tumors and its expression is associated with advanced tumor stage, metastasis, and poor survival. However, the underlying mechanisms of C1GALT1 in HCC malignancy remain unclear. In this study, we found that overexpression of C1GALT1 enhanced HCC cell adhesion to extracellular matrix (ECM) proteins, migration, and invasion, whereas RNAi-mediated knockdown of C1GALT1 suppressed these phenotypes. The promoting effect of C1GALT1 on the metastasis of HCC cells was demonstrated in a mouse xenograft model. Mechanistic investigations showed that the C1GALT1-enhanced phenotypic changes in HCC cells were significantly suppressed by anti-integrin β1 blocking antibody. Moreover, C1GALT1 was able to modify O-glycans on integrin β1 and regulate integrin β1 activity as well as its downstream signaling. These results suggest that C1GALT1 could enhance HCC invasiveness through integrin β1 and provide novel insights into the roles of O-glycosylation in HCC metastasis.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>25089569</pmid><doi>10.1371/journal.pone.0094995</doi><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2014-08, Vol.9 (8), p.e94995-e94995 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1551148454 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS) Journals Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Animals Antibodies, Neutralizing - pharmacology Antigens Biology and Life Sciences Blocking antibodies Carcinoma, Hepatocellular - drug therapy Carcinoma, Hepatocellular - genetics Carcinoma, Hepatocellular - metabolism Carcinoma, Hepatocellular - secondary Cell adhesion Cell adhesion & migration Cell Adhesion - drug effects Cell cycle Cell growth Cell Line, Tumor Cell Movement - drug effects Cloning Developmental biology Experiments Extracellular matrix Extracellular Matrix Proteins - genetics Extracellular Matrix Proteins - metabolism Female Galactosyltransferases - antagonists & inhibitors Galactosyltransferases - genetics Galactosyltransferases - metabolism Gene expression Gene Expression Regulation, Neoplastic Glycosylation Hepatocellular carcinoma Hepatology Humans Immunoglobulins Integrin beta1 - genetics Integrin beta1 - metabolism Invasiveness Kinases Liver cancer Liver Neoplasms, Experimental - drug therapy Liver Neoplasms, Experimental - genetics Liver Neoplasms, Experimental - metabolism Liver Neoplasms, Experimental - pathology Lung Neoplasms - drug therapy Lung Neoplasms - genetics Lung Neoplasms - metabolism Lung Neoplasms - secondary Malignancy Medicine Medicine and Health Sciences Metastases Metastasis Mice Mice, SCID Neoplasm Invasiveness Physical Sciences Polysaccharides Polysaccharides - chemistry Polysaccharides - metabolism Protein Binding Proteins RNA, Small Interfering - genetics RNA, Small Interfering - metabolism RNA-mediated interference Signal Transduction Signaling Surgery Tumors Xenografts Xenotransplantation |
| title | C1GALT1 promotes invasive phenotypes of hepatocellular carcinoma cells by modulating integrin β1 glycosylation and activity |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-16T06%3A16%3A07IST&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=C1GALT1%20promotes%20invasive%20phenotypes%20of%20hepatocellular%20carcinoma%20cells%20by%20modulating%20integrin%20%CE%B21%20glycosylation%20and%20activity&rft.jtitle=PloS%20one&rft.au=Liu,%20Chiung-Hui&rft.date=2014-08-04&rft.volume=9&rft.issue=8&rft.spage=e94995&rft.epage=e94995&rft.pages=e94995-e94995&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0094995&rft_dat=%3Cproquest_plos_%3E1551608584%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=1551148454&rft_id=info:pmid/25089569&rft_doaj_id=oai_doaj_org_article_e413e7d74f5948ddbec85a24b2f1749f&rfr_iscdi=true |