Cooperative roles for emmprin and LYVE-1 in the regulation of chemoresistance for primary effusion lymphoma
The Kaposi's sarcoma-associated herpesvirus is the causative agent of primary effusion lymphoma (PEL), for which cytotoxic chemotherapy represents the standard of care. The high mortality associated with PEL may be explained in part by resistance of these tumors to chemotherapy. The membrane-bo...
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| description | The Kaposi's sarcoma-associated herpesvirus is the causative agent of primary effusion lymphoma (PEL), for which cytotoxic chemotherapy represents the standard of care. The high mortality associated with PEL may be explained in part by resistance of these tumors to chemotherapy. The membrane-bound glycoprotein emmprin (CD147) enhances chemoresistance in tumors through effects on transporter expression, trafficking and interactions. Interactions between hyaluronan and hyaluronan receptors on the cell surface also facilitate emmprin-mediated chemoresistance. Whether emmprin or hyaluronan-receptor interactions regulate chemotherapeutic resistance for virus-associated malignancies is unknown. Using human PEL tumor cells, we found that PEL sensitivity to chemotherapy is directly proportional to expression of emmprin, the lymphatic vessel endothelial hyaluronan receptor-1 (LYVE-1) and a drug transporter known as the breast cancer resistance protein/ABCG2 (BCRP), and that emmprin, LYVE-1 and BCRP interact with each other and colocalize on the PEL cell surface. In addition, we found that emmprin induces chemoresistance in PEL cells through upregulation of BCRP expression, and RNA interference targeting of emmprin, LYVE-1 or BCRP enhances PEL cell apoptosis induced by chemotherapy. Finally, disruption of hyaluronan-receptor interactions using small hyaluronan oligosaccharides reduces expression of emmprin and BCRP while sensitizing PEL cells to chemotherapy. Collectively, these data support interdependent roles for emmprin, LYVE-1 and BCRP in chemotherapeutic resistance for PEL. |
| doi_str_mv | 10.1038/leu.2011.144 |
| format | Article |
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The high mortality associated with PEL may be explained in part by resistance of these tumors to chemotherapy. The membrane-bound glycoprotein emmprin (CD147) enhances chemoresistance in tumors through effects on transporter expression, trafficking and interactions. Interactions between hyaluronan and hyaluronan receptors on the cell surface also facilitate emmprin-mediated chemoresistance. Whether emmprin or hyaluronan-receptor interactions regulate chemotherapeutic resistance for virus-associated malignancies is unknown. Using human PEL tumor cells, we found that PEL sensitivity to chemotherapy is directly proportional to expression of emmprin, the lymphatic vessel endothelial hyaluronan receptor-1 (LYVE-1) and a drug transporter known as the breast cancer resistance protein/ABCG2 (BCRP), and that emmprin, LYVE-1 and BCRP interact with each other and colocalize on the PEL cell surface. In addition, we found that emmprin induces chemoresistance in PEL cells through upregulation of BCRP expression, and RNA interference targeting of emmprin, LYVE-1 or BCRP enhances PEL cell apoptosis induced by chemotherapy. Finally, disruption of hyaluronan-receptor interactions using small hyaluronan oligosaccharides reduces expression of emmprin and BCRP while sensitizing PEL cells to chemotherapy. Collectively, these data support interdependent roles for emmprin, LYVE-1 and BCRP in chemotherapeutic resistance for PEL.</description><identifier>ISSN: 0887-6924</identifier><identifier>EISSN: 1476-5551</identifier><identifier>DOI: 10.1038/leu.2011.144</identifier><identifier>PMID: 21660043</identifier><identifier>CODEN: LEUKED</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>692/699/67/1059/2326 ; 692/699/67/1990/291/1621/1915 ; Antineoplastic Agents - therapeutic use ; Apoptosis ; Base Sequence ; Basigin - physiology ; Biological and medical sciences ; Breast cancer ; Cancer ; Cancer Research ; Cancer therapies ; Care and treatment ; CD147 antigen ; Cell Line, Tumor ; Cell surface ; Cells ; Chemoresistance ; Chemotherapy ; Critical Care Medicine ; Cytotoxicity ; Disease resistance ; DNA Primers ; Drug resistance ; Drug Resistance, Neoplasm ; Effusion ; Flow Cytometry ; Fluorescent Antibody Technique ; Gene expression ; Glycoproteins ; Health aspects ; Hematologic and hematopoietic diseases ; Hematology ; Herpes viruses ; Human herpesvirus 8 ; Humans ; Hyaluronic acid ; Intensive ; Internal Medicine ; Kaposi's sarcoma ; Kaposis sarcoma ; Laboratories ; Leukemia ; Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis ; Lymphoma ; Lymphoma, Primary Effusion - drug therapy ; Lymphoma, Primary Effusion - physiopathology ; Lymphomas ; Medical prognosis ; Medical sciences ; Medicine ; Medicine & Public Health ; Mortality ; Oligosaccharides ; Oncology ; original-article ; Primary effusion lymphoma ; Real-Time Polymerase Chain Reaction ; Receptors ; Risk factors ; RNA Interference ; RNA-mediated interference ; Sarcoma ; Sensitizing ; Signal transduction ; Tumor cells ; Tumors ; United States ; Vesicular Transport Proteins - physiology ; Viruses</subject><ispartof>Leukemia, 2011-10, Vol.25 (10), p.1598-1609</ispartof><rights>Macmillan Publishers Limited 2011</rights><rights>2015 INIST-CNRS</rights><rights>COPYRIGHT 2011 Nature Publishing Group</rights><rights>Macmillan Publishers Limited 2011.</rights><rights>Copyright Nature Publishing Group Oct 2011</rights><rights>2011 Macmillan Publishers Limited All rights reserved 2011</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c727t-3423b28e530ee59db0a8d1aa353394ab24b7d911bca1e342e2ece5a8959613d93</citedby><cites>FETCH-LOGICAL-c727t-3423b28e530ee59db0a8d1aa353394ab24b7d911bca1e342e2ece5a8959613d93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/leu.2011.144$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/leu.2011.144$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,314,780,784,885,2727,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=24628663$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21660043$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Qin, Z</creatorcontrib><creatorcontrib>Dai, L</creatorcontrib><creatorcontrib>Bratoeva, M</creatorcontrib><creatorcontrib>Slomiany, M G</creatorcontrib><creatorcontrib>Toole, B P</creatorcontrib><creatorcontrib>Parsons, C</creatorcontrib><title>Cooperative roles for emmprin and LYVE-1 in the regulation of chemoresistance for primary effusion lymphoma</title><title>Leukemia</title><addtitle>Leukemia</addtitle><addtitle>Leukemia</addtitle><description>The Kaposi's sarcoma-associated herpesvirus is the causative agent of primary effusion lymphoma (PEL), for which cytotoxic chemotherapy represents the standard of care. The high mortality associated with PEL may be explained in part by resistance of these tumors to chemotherapy. The membrane-bound glycoprotein emmprin (CD147) enhances chemoresistance in tumors through effects on transporter expression, trafficking and interactions. Interactions between hyaluronan and hyaluronan receptors on the cell surface also facilitate emmprin-mediated chemoresistance. Whether emmprin or hyaluronan-receptor interactions regulate chemotherapeutic resistance for virus-associated malignancies is unknown. Using human PEL tumor cells, we found that PEL sensitivity to chemotherapy is directly proportional to expression of emmprin, the lymphatic vessel endothelial hyaluronan receptor-1 (LYVE-1) and a drug transporter known as the breast cancer resistance protein/ABCG2 (BCRP), and that emmprin, LYVE-1 and BCRP interact with each other and colocalize on the PEL cell surface. In addition, we found that emmprin induces chemoresistance in PEL cells through upregulation of BCRP expression, and RNA interference targeting of emmprin, LYVE-1 or BCRP enhances PEL cell apoptosis induced by chemotherapy. Finally, disruption of hyaluronan-receptor interactions using small hyaluronan oligosaccharides reduces expression of emmprin and BCRP while sensitizing PEL cells to chemotherapy. 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Malignant lymphomas. Malignant reticulosis. Myelofibrosis</subject><subject>Lymphoma</subject><subject>Lymphoma, Primary Effusion - drug therapy</subject><subject>Lymphoma, Primary Effusion - physiopathology</subject><subject>Lymphomas</subject><subject>Medical prognosis</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mortality</subject><subject>Oligosaccharides</subject><subject>Oncology</subject><subject>original-article</subject><subject>Primary effusion lymphoma</subject><subject>Real-Time Polymerase Chain Reaction</subject><subject>Receptors</subject><subject>Risk factors</subject><subject>RNA Interference</subject><subject>RNA-mediated interference</subject><subject>Sarcoma</subject><subject>Sensitizing</subject><subject>Signal transduction</subject><subject>Tumor cells</subject><subject>Tumors</subject><subject>United States</subject><subject>Vesicular Transport Proteins - physiology</subject><subject>Viruses</subject><issn>0887-6924</issn><issn>1476-5551</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</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><recordid>eNp10s2L1DAYB-Aiijuu3jxLUNSLHfPVNL0Iy7B-wIAXFTyFNH077Zoms0m7sP-9qTPO7IhLD6XJ875Jk1-WPSd4STCT7y1MS4oJWRLOH2QLwkuRF0VBHmYLLGWZi4rys-xJjFcYz5PicXZGiRAYc7bIfq2830LQY38DKHgLEbU-IBiGbegd0q5B658_LnOC0tfYJQObySbuHfItMh0MPkDs46idgT-1qXDQ4RZB205xdvZ22HZ-0E-zR622EZ7t3-fZ94-X31af8_XXT19WF-vclLQcc8Ypq6mEgmGAompqrGVDtGYFYxXXNeV12VSE1EYTSBgoGCi0rIpKENZU7Dz7sOu7neoBGgNuDNqq_b6U1706nXF9pzb-RjEhmeAyNXi7bxD89QRxVEMfDVirHfgpqkpIIiqOSZIv_5FXfgou_Z2SVckxxaJI6NV9iApelIyXlB7VRltQvWt92puZF1YXtMSsTHcqklr-R6WngaE33kHbp_GTgjd3CjrQduyit9N8g_EUvttBE3yMAdrDgRGs5qSplDQ1J02lpCX-4u4hH_DfaCXweg90NNq2IQWkj0fHBZVCzC7fuTgnbgPheDr3LIx23ulxCnBomNBsZvIbgIHzqg</recordid><startdate>20111001</startdate><enddate>20111001</enddate><creator>Qin, Z</creator><creator>Dai, L</creator><creator>Bratoeva, M</creator><creator>Slomiany, M G</creator><creator>Toole, B P</creator><creator>Parsons, C</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>IQODW</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>3V.</scope><scope>7QL</scope><scope>7RV</scope><scope>7T5</scope><scope>7T7</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</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>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>5PM</scope></search><sort><creationdate>20111001</creationdate><title>Cooperative roles for emmprin and LYVE-1 in the regulation of chemoresistance for primary effusion lymphoma</title><author>Qin, Z ; 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Malignant lymphomas. Malignant reticulosis. 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lymphoma</atitle><jtitle>Leukemia</jtitle><stitle>Leukemia</stitle><addtitle>Leukemia</addtitle><date>2011-10-01</date><risdate>2011</risdate><volume>25</volume><issue>10</issue><spage>1598</spage><epage>1609</epage><pages>1598-1609</pages><issn>0887-6924</issn><eissn>1476-5551</eissn><coden>LEUKED</coden><abstract>The Kaposi's sarcoma-associated herpesvirus is the causative agent of primary effusion lymphoma (PEL), for which cytotoxic chemotherapy represents the standard of care. The high mortality associated with PEL may be explained in part by resistance of these tumors to chemotherapy. The membrane-bound glycoprotein emmprin (CD147) enhances chemoresistance in tumors through effects on transporter expression, trafficking and interactions. Interactions between hyaluronan and hyaluronan receptors on the cell surface also facilitate emmprin-mediated chemoresistance. Whether emmprin or hyaluronan-receptor interactions regulate chemotherapeutic resistance for virus-associated malignancies is unknown. Using human PEL tumor cells, we found that PEL sensitivity to chemotherapy is directly proportional to expression of emmprin, the lymphatic vessel endothelial hyaluronan receptor-1 (LYVE-1) and a drug transporter known as the breast cancer resistance protein/ABCG2 (BCRP), and that emmprin, LYVE-1 and BCRP interact with each other and colocalize on the PEL cell surface. In addition, we found that emmprin induces chemoresistance in PEL cells through upregulation of BCRP expression, and RNA interference targeting of emmprin, LYVE-1 or BCRP enhances PEL cell apoptosis induced by chemotherapy. Finally, disruption of hyaluronan-receptor interactions using small hyaluronan oligosaccharides reduces expression of emmprin and BCRP while sensitizing PEL cells to chemotherapy. Collectively, these data support interdependent roles for emmprin, LYVE-1 and BCRP in chemotherapeutic resistance for PEL.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>21660043</pmid><doi>10.1038/leu.2011.144</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Nature; EZB-FREE-00999 freely available EZB journals; SpringerLink Journals - AutoHoldings |
| subjects | 692/699/67/1059/2326 692/699/67/1990/291/1621/1915 Antineoplastic Agents - therapeutic use Apoptosis Base Sequence Basigin - physiology Biological and medical sciences Breast cancer Cancer Cancer Research Cancer therapies Care and treatment CD147 antigen Cell Line, Tumor Cell surface Cells Chemoresistance Chemotherapy Critical Care Medicine Cytotoxicity Disease resistance DNA Primers Drug resistance Drug Resistance, Neoplasm Effusion Flow Cytometry Fluorescent Antibody Technique Gene expression Glycoproteins Health aspects Hematologic and hematopoietic diseases Hematology Herpes viruses Human herpesvirus 8 Humans Hyaluronic acid Intensive Internal Medicine Kaposi's sarcoma Kaposis sarcoma Laboratories Leukemia Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis Lymphoma Lymphoma, Primary Effusion - drug therapy Lymphoma, Primary Effusion - physiopathology Lymphomas Medical prognosis Medical sciences Medicine Medicine & Public Health Mortality Oligosaccharides Oncology original-article Primary effusion lymphoma Real-Time Polymerase Chain Reaction Receptors Risk factors RNA Interference RNA-mediated interference Sarcoma Sensitizing Signal transduction Tumor cells Tumors United States Vesicular Transport Proteins - physiology Viruses |
| title | Cooperative roles for emmprin and LYVE-1 in the regulation of chemoresistance for primary effusion lymphoma |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-07T06%3A10%3A15IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Cooperative%20roles%20for%20emmprin%20and%20LYVE-1%20in%20the%20regulation%20of%20chemoresistance%20for%20primary%20effusion%20lymphoma&rft.jtitle=Leukemia&rft.au=Qin,%20Z&rft.date=2011-10-01&rft.volume=25&rft.issue=10&rft.spage=1598&rft.epage=1609&rft.pages=1598-1609&rft.issn=0887-6924&rft.eissn=1476-5551&rft.coden=LEUKED&rft_id=info:doi/10.1038/leu.2011.144&rft_dat=%3Cgale_pubme%3EA270375516%3C/gale_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2645734722&rft_id=info:pmid/21660043&rft_galeid=A270375516&rfr_iscdi=true |