Upregulation of the mevalonate pathway by cholesterol depletion abolishes tolerance to N-bisphosphonate induced V[gamma]9V[delta]2 T cell cytotoxicity in PC-3 prostate cancer cells
Zoledronate (ZOL) inhibits farnesyl pyrophosphate synthase leading to intracellular accumulation of isopentenyl pyrophosphate/triphosphoric acid 1-adenosin-5'-yl ester 3-(3-methylbut-3-enyl) ester (IPP/ApppI). Cytotoxic Vγ9Vδ2 T cells have been shown to recognize IPP/ApppI in breast cancer cell...
Gespeichert in:
| Veröffentlicht in: | Cancer letters 2015-02, Vol.357 (1), p.279 |
|---|---|
| Hauptverfasser: | , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | |
|---|---|
| container_issue | 1 |
| container_start_page | 279 |
| container_title | Cancer letters |
| container_volume | 357 |
| creator | Arkko, S Zlatev, HP Mönkkönen, H Räikkönen, J Benzaïd, I Clézardin, P Mönkkönen, J Määttä, JA |
| description | Zoledronate (ZOL) inhibits farnesyl pyrophosphate synthase leading to intracellular accumulation of isopentenyl pyrophosphate/triphosphoric acid 1-adenosin-5'-yl ester 3-(3-methylbut-3-enyl) ester (IPP/ApppI). Cytotoxic Vγ9Vδ2 T cells have been shown to recognize IPP/ApppI in breast cancer cells. Further, human breast cancer cells have been shown to differ remarkably in their ZOL treatment induced IPP/ApppI production and responses to that. In this communication we analysed the responsiveness of prostate cancer cells PC-3 and DU-145, Caki-2 renal carcinoma cells and U87MG glioblastoma cells to ZOL treatment, and the subsequent activation of Vγ9Vδ2 T-cell cytotoxicity. Of the cell lines tested, PC-3 cells were not susceptible to Vγ9Vδ2 T-cell cytotoxicity due to low activity of the mevalonate pathway and low amount of IPP formed. However, the resistance of PC-3 cells to Vγ9Vδ2 T-cell cytotoxicity could be abrogated by upregulation of the mevalonate pathway through cholesterol depletion. |
| doi_str_mv | 10.1016/j.canlet.2014.11.030 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest</sourceid><recordid>TN_cdi_proquest_journals_1641261730</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>3541579161</sourcerecordid><originalsourceid>FETCH-proquest_journals_16412617303</originalsourceid><addsrcrecordid>eNqNjk1OwzAQhS0EEuXnBixGYp1gx_nrugKxQl2Ubqqqcpxp48iJg-0AuRcHxKk4AIvRjOZ9780Q8sBozCjLn9pYil6jjxPK0pixmHJ6QRasLJKoWJb0kizCJo14ybNrcuNcSynN0iJbkJ_3weJp1MIr04M5gm8QOvwU2vTCIwzCN19igmoC2RiNzqM1Gmocwr3ZIiqjlWvQgQ-yFb3EMMFbVCk3NGauc5Dq61FiDdvdSXSd2C-3uxq1F_sENiBRa5CTN958K6n8FHBYryIOgzXOz345J9sz6e7I1VFoh_d__ZY8vjxvVq9RoD_G8OOhNaPtg3RgecqSnBWc8v9Rv0ShbPA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1641261730</pqid></control><display><type>article</type><title>Upregulation of the mevalonate pathway by cholesterol depletion abolishes tolerance to N-bisphosphonate induced V[gamma]9V[delta]2 T cell cytotoxicity in PC-3 prostate cancer cells</title><source>Elsevier ScienceDirect Journals Complete</source><creator>Arkko, S ; Zlatev, HP ; Mönkkönen, H ; Räikkönen, J ; Benzaïd, I ; Clézardin, P ; Mönkkönen, J ; Määttä, JA</creator><creatorcontrib>Arkko, S ; Zlatev, HP ; Mönkkönen, H ; Räikkönen, J ; Benzaïd, I ; Clézardin, P ; Mönkkönen, J ; Määttä, JA</creatorcontrib><description>Zoledronate (ZOL) inhibits farnesyl pyrophosphate synthase leading to intracellular accumulation of isopentenyl pyrophosphate/triphosphoric acid 1-adenosin-5'-yl ester 3-(3-methylbut-3-enyl) ester (IPP/ApppI). Cytotoxic Vγ9Vδ2 T cells have been shown to recognize IPP/ApppI in breast cancer cells. Further, human breast cancer cells have been shown to differ remarkably in their ZOL treatment induced IPP/ApppI production and responses to that. In this communication we analysed the responsiveness of prostate cancer cells PC-3 and DU-145, Caki-2 renal carcinoma cells and U87MG glioblastoma cells to ZOL treatment, and the subsequent activation of Vγ9Vδ2 T-cell cytotoxicity. Of the cell lines tested, PC-3 cells were not susceptible to Vγ9Vδ2 T-cell cytotoxicity due to low activity of the mevalonate pathway and low amount of IPP formed. However, the resistance of PC-3 cells to Vγ9Vδ2 T-cell cytotoxicity could be abrogated by upregulation of the mevalonate pathway through cholesterol depletion.</description><identifier>ISSN: 0304-3835</identifier><identifier>EISSN: 1872-7980</identifier><identifier>DOI: 10.1016/j.canlet.2014.11.030</identifier><language>eng</language><publisher>Clare: Elsevier Limited</publisher><subject>Breast cancer ; Drug resistance ; Immunotherapy ; Prostate cancer</subject><ispartof>Cancer letters, 2015-02, Vol.357 (1), p.279</ispartof><rights>Copyright Elsevier Limited Feb 1, 2015</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids></links><search><creatorcontrib>Arkko, S</creatorcontrib><creatorcontrib>Zlatev, HP</creatorcontrib><creatorcontrib>Mönkkönen, H</creatorcontrib><creatorcontrib>Räikkönen, J</creatorcontrib><creatorcontrib>Benzaïd, I</creatorcontrib><creatorcontrib>Clézardin, P</creatorcontrib><creatorcontrib>Mönkkönen, J</creatorcontrib><creatorcontrib>Määttä, JA</creatorcontrib><title>Upregulation of the mevalonate pathway by cholesterol depletion abolishes tolerance to N-bisphosphonate induced V[gamma]9V[delta]2 T cell cytotoxicity in PC-3 prostate cancer cells</title><title>Cancer letters</title><description>Zoledronate (ZOL) inhibits farnesyl pyrophosphate synthase leading to intracellular accumulation of isopentenyl pyrophosphate/triphosphoric acid 1-adenosin-5'-yl ester 3-(3-methylbut-3-enyl) ester (IPP/ApppI). Cytotoxic Vγ9Vδ2 T cells have been shown to recognize IPP/ApppI in breast cancer cells. Further, human breast cancer cells have been shown to differ remarkably in their ZOL treatment induced IPP/ApppI production and responses to that. In this communication we analysed the responsiveness of prostate cancer cells PC-3 and DU-145, Caki-2 renal carcinoma cells and U87MG glioblastoma cells to ZOL treatment, and the subsequent activation of Vγ9Vδ2 T-cell cytotoxicity. Of the cell lines tested, PC-3 cells were not susceptible to Vγ9Vδ2 T-cell cytotoxicity due to low activity of the mevalonate pathway and low amount of IPP formed. However, the resistance of PC-3 cells to Vγ9Vδ2 T-cell cytotoxicity could be abrogated by upregulation of the mevalonate pathway through cholesterol depletion.</description><subject>Breast cancer</subject><subject>Drug resistance</subject><subject>Immunotherapy</subject><subject>Prostate cancer</subject><issn>0304-3835</issn><issn>1872-7980</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><recordid>eNqNjk1OwzAQhS0EEuXnBixGYp1gx_nrugKxQl2Ubqqqcpxp48iJg-0AuRcHxKk4AIvRjOZ9780Q8sBozCjLn9pYil6jjxPK0pixmHJ6QRasLJKoWJb0kizCJo14ybNrcuNcSynN0iJbkJ_3weJp1MIr04M5gm8QOvwU2vTCIwzCN19igmoC2RiNzqM1Gmocwr3ZIiqjlWvQgQ-yFb3EMMFbVCk3NGauc5Dq61FiDdvdSXSd2C-3uxq1F_sENiBRa5CTN958K6n8FHBYryIOgzXOz345J9sz6e7I1VFoh_d__ZY8vjxvVq9RoD_G8OOhNaPtg3RgecqSnBWc8v9Rv0ShbPA</recordid><startdate>20150201</startdate><enddate>20150201</enddate><creator>Arkko, S</creator><creator>Zlatev, HP</creator><creator>Mönkkönen, H</creator><creator>Räikkönen, J</creator><creator>Benzaïd, I</creator><creator>Clézardin, P</creator><creator>Mönkkönen, J</creator><creator>Määttä, JA</creator><general>Elsevier Limited</general><scope>7TO</scope><scope>7U9</scope><scope>H94</scope><scope>K9.</scope><scope>NAPCQ</scope></search><sort><creationdate>20150201</creationdate><title>Upregulation of the mevalonate pathway by cholesterol depletion abolishes tolerance to N-bisphosphonate induced V[gamma]9V[delta]2 T cell cytotoxicity in PC-3 prostate cancer cells</title><author>Arkko, S ; Zlatev, HP ; Mönkkönen, H ; Räikkönen, J ; Benzaïd, I ; Clézardin, P ; Mönkkönen, J ; Määttä, JA</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-proquest_journals_16412617303</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Breast cancer</topic><topic>Drug resistance</topic><topic>Immunotherapy</topic><topic>Prostate cancer</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Arkko, S</creatorcontrib><creatorcontrib>Zlatev, HP</creatorcontrib><creatorcontrib>Mönkkönen, H</creatorcontrib><creatorcontrib>Räikkönen, J</creatorcontrib><creatorcontrib>Benzaïd, I</creatorcontrib><creatorcontrib>Clézardin, P</creatorcontrib><creatorcontrib>Mönkkönen, J</creatorcontrib><creatorcontrib>Määttä, JA</creatorcontrib><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><jtitle>Cancer letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Arkko, S</au><au>Zlatev, HP</au><au>Mönkkönen, H</au><au>Räikkönen, J</au><au>Benzaïd, I</au><au>Clézardin, P</au><au>Mönkkönen, J</au><au>Määttä, JA</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Upregulation of the mevalonate pathway by cholesterol depletion abolishes tolerance to N-bisphosphonate induced V[gamma]9V[delta]2 T cell cytotoxicity in PC-3 prostate cancer cells</atitle><jtitle>Cancer letters</jtitle><date>2015-02-01</date><risdate>2015</risdate><volume>357</volume><issue>1</issue><spage>279</spage><pages>279-</pages><issn>0304-3835</issn><eissn>1872-7980</eissn><abstract>Zoledronate (ZOL) inhibits farnesyl pyrophosphate synthase leading to intracellular accumulation of isopentenyl pyrophosphate/triphosphoric acid 1-adenosin-5'-yl ester 3-(3-methylbut-3-enyl) ester (IPP/ApppI). Cytotoxic Vγ9Vδ2 T cells have been shown to recognize IPP/ApppI in breast cancer cells. Further, human breast cancer cells have been shown to differ remarkably in their ZOL treatment induced IPP/ApppI production and responses to that. In this communication we analysed the responsiveness of prostate cancer cells PC-3 and DU-145, Caki-2 renal carcinoma cells and U87MG glioblastoma cells to ZOL treatment, and the subsequent activation of Vγ9Vδ2 T-cell cytotoxicity. Of the cell lines tested, PC-3 cells were not susceptible to Vγ9Vδ2 T-cell cytotoxicity due to low activity of the mevalonate pathway and low amount of IPP formed. However, the resistance of PC-3 cells to Vγ9Vδ2 T-cell cytotoxicity could be abrogated by upregulation of the mevalonate pathway through cholesterol depletion.</abstract><cop>Clare</cop><pub>Elsevier Limited</pub><doi>10.1016/j.canlet.2014.11.030</doi></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0304-3835 |
| ispartof | Cancer letters, 2015-02, Vol.357 (1), p.279 |
| issn | 0304-3835 1872-7980 |
| language | eng |
| recordid | cdi_proquest_journals_1641261730 |
| source | Elsevier ScienceDirect Journals Complete |
| subjects | Breast cancer Drug resistance Immunotherapy Prostate cancer |
| title | Upregulation of the mevalonate pathway by cholesterol depletion abolishes tolerance to N-bisphosphonate induced V[gamma]9V[delta]2 T cell cytotoxicity in PC-3 prostate cancer cells |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-05T11%3A10%3A50IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Upregulation%20of%20the%20mevalonate%20pathway%20by%20cholesterol%20depletion%20abolishes%20tolerance%20to%20N-bisphosphonate%20induced%20V%5Bgamma%5D9V%5Bdelta%5D2%20T%20cell%20cytotoxicity%20in%20PC-3%20prostate%20cancer%20cells&rft.jtitle=Cancer%20letters&rft.au=Arkko,%20S&rft.date=2015-02-01&rft.volume=357&rft.issue=1&rft.spage=279&rft.pages=279-&rft.issn=0304-3835&rft.eissn=1872-7980&rft_id=info:doi/10.1016/j.canlet.2014.11.030&rft_dat=%3Cproquest%3E3541579161%3C/proquest%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1641261730&rft_id=info:pmid/&rfr_iscdi=true |