Imatinib and nilotinib reverse multidrug resistance in cancer cells by inhibiting the efflux activity of the MRP7 (ABCC10)
One of the major mechanisms that could produce resistance to antineoplastic drugs in cancer cells is the ATP binding cassette (ABC) transporters. The ABC transporters can significantly decrease the intracellular concentration of antineoplastic drugs by increasing their efflux, thereby lowering the c...
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| creator | Shen, Tong Kuang, Ye-Hong Ashby, Charles R Lei, Yu Chen, Angel Zhou, Ying Chen, Xiang Tiwari, Amit K Hopper-Borge, Elizabeth Ouyang, Jiangyong Chen, Zhe-Sheng |
| description | One of the major mechanisms that could produce resistance to antineoplastic drugs in cancer cells is the ATP binding cassette (ABC) transporters. The ABC transporters can significantly decrease the intracellular concentration of antineoplastic drugs by increasing their efflux, thereby lowering the cytotoxic activity of antineoplastic drugs. One of these transporters, the multiple resistant protein 7 (MRP7, ABCC10), has recently been shown to produce resistance to antineoplastic drugs by increasing the efflux of paclitaxel. In this study, we examined the effects of BCR-Abl tyrosine kinase inhibitors imatinib, nilotinib and dasatinib on the activity and expression of MRP7 in HEK293 cells transfected with MRP7, designated HEK-MRP7-2.
We report for the first time that imatinib and nilotinib reversed MRP7-mediated multidrug resistance. Our MTT assay results indicated that MRP7 expression in HEK-MRP7-2 cells was not significantly altered by incubation with 5 microM of imatinib or nilotinib for up to 72 hours. In addition, imatinib and nilotinib (1-5 microM) produced a significant concentration-dependent reversal of MRP7-mediated multidrug resistance by enhancing the sensitivity of HEK-MRP7-2 cells to paclitaxel and vincristine. Imatinib and nilotinib, at 5 microM, significantly increased the accumulation of [(3)H]-paclitaxel in HEK-MRP7-2 cells. The incubation of the HEK-MRP7-2 cells with imatinib or nilotinib (5 microM) also significantly inhibited the efflux of paclitaxel.
Imatinib and nilotinib reverse MRP7-mediated paclitaxel resistance, most likely due to their inhibition of the efflux of paclitaxel via MRP7. These findings suggest that imatinib or nilotinib, in combination with other antineoplastic drugs, may be useful in the treatment of certain resistant cancers. |
| doi_str_mv | 10.1371/journal.pone.0007520 |
| format | Article |
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We report for the first time that imatinib and nilotinib reversed MRP7-mediated multidrug resistance. Our MTT assay results indicated that MRP7 expression in HEK-MRP7-2 cells was not significantly altered by incubation with 5 microM of imatinib or nilotinib for up to 72 hours. In addition, imatinib and nilotinib (1-5 microM) produced a significant concentration-dependent reversal of MRP7-mediated multidrug resistance by enhancing the sensitivity of HEK-MRP7-2 cells to paclitaxel and vincristine. Imatinib and nilotinib, at 5 microM, significantly increased the accumulation of [(3)H]-paclitaxel in HEK-MRP7-2 cells. The incubation of the HEK-MRP7-2 cells with imatinib or nilotinib (5 microM) also significantly inhibited the efflux of paclitaxel.
Imatinib and nilotinib reverse MRP7-mediated paclitaxel resistance, most likely due to their inhibition of the efflux of paclitaxel via MRP7. These findings suggest that imatinib or nilotinib, in combination with other antineoplastic drugs, may be useful in the treatment of certain resistant cancers.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0007520</identifier><identifier>PMID: 19841739</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Abl protein ; Antineoplastic agents ; Antineoplastic Agents - pharmacology ; Antineoplastic drugs ; BCR protein ; BCR-ABL protein ; Benzamides ; Binding sites ; Cancer ; Cancer cells ; Cancer therapies ; Cell Line ; Chemotherapy ; Competition ; Cytotoxicity ; Dermatology ; Dose-Response Relationship, Drug ; Drug resistance ; Drug Resistance, Multiple ; Drug Resistance, Neoplasm ; Drugs ; Efflux ; Fusion protein ; Gene Expression Regulation, Neoplastic ; Humans ; Imatinib ; Imatinib Mesylate ; Inhibitor drugs ; Kinases ; Laboratories ; Leukemia ; Microbial drug resistance ; Models, Chemical ; Multidrug resistance ; Multidrug Resistance-Associated Proteins - genetics ; Multidrug Resistance-Associated Proteins - metabolism ; Multidrug resistant organisms ; Neoplasms - drug therapy ; Neoplasms - metabolism ; Paclitaxel ; Paclitaxel - pharmacology ; Pharmaceutical sciences ; Pharmacology/Drug Development ; Pharmacology/Drug Interactions ; Pharmacology/Drug Resistance ; Pharmacy ; Piperazines - pharmacology ; Protein-tyrosine kinase ; Proteins ; Pyrimidines - pharmacology ; Sensitivity enhancement ; Stem cells ; Targeted cancer therapy ; Tetrazolium Salts - pharmacology ; Thiazoles - pharmacology ; Tyrosine ; Vincristine</subject><ispartof>PloS one, 2009-10, Vol.4 (10), p.e7520</ispartof><rights>COPYRIGHT 2009 Public Library of Science</rights><rights>2009 Shen et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (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>Shen et al. 2009</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c663t-f1bc6364372dddfe276ff37937e5ce45c289bafd0fe8875fd4587ceefc3500843</citedby><cites>FETCH-LOGICAL-c663t-f1bc6364372dddfe276ff37937e5ce45c289bafd0fe8875fd4587ceefc3500843</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/PMC2759525/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2759525/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2100,2926,23865,27923,27924,53790,53792,79371,79372</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19841739$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Fox, Debbie</contributor><creatorcontrib>Shen, Tong</creatorcontrib><creatorcontrib>Kuang, Ye-Hong</creatorcontrib><creatorcontrib>Ashby, Charles R</creatorcontrib><creatorcontrib>Lei, Yu</creatorcontrib><creatorcontrib>Chen, Angel</creatorcontrib><creatorcontrib>Zhou, Ying</creatorcontrib><creatorcontrib>Chen, Xiang</creatorcontrib><creatorcontrib>Tiwari, Amit K</creatorcontrib><creatorcontrib>Hopper-Borge, Elizabeth</creatorcontrib><creatorcontrib>Ouyang, Jiangyong</creatorcontrib><creatorcontrib>Chen, Zhe-Sheng</creatorcontrib><title>Imatinib and nilotinib reverse multidrug resistance in cancer cells by inhibiting the efflux activity of the MRP7 (ABCC10)</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>One of the major mechanisms that could produce resistance to antineoplastic drugs in cancer cells is the ATP binding cassette (ABC) transporters. The ABC transporters can significantly decrease the intracellular concentration of antineoplastic drugs by increasing their efflux, thereby lowering the cytotoxic activity of antineoplastic drugs. One of these transporters, the multiple resistant protein 7 (MRP7, ABCC10), has recently been shown to produce resistance to antineoplastic drugs by increasing the efflux of paclitaxel. In this study, we examined the effects of BCR-Abl tyrosine kinase inhibitors imatinib, nilotinib and dasatinib on the activity and expression of MRP7 in HEK293 cells transfected with MRP7, designated HEK-MRP7-2.
We report for the first time that imatinib and nilotinib reversed MRP7-mediated multidrug resistance. Our MTT assay results indicated that MRP7 expression in HEK-MRP7-2 cells was not significantly altered by incubation with 5 microM of imatinib or nilotinib for up to 72 hours. In addition, imatinib and nilotinib (1-5 microM) produced a significant concentration-dependent reversal of MRP7-mediated multidrug resistance by enhancing the sensitivity of HEK-MRP7-2 cells to paclitaxel and vincristine. Imatinib and nilotinib, at 5 microM, significantly increased the accumulation of [(3)H]-paclitaxel in HEK-MRP7-2 cells. The incubation of the HEK-MRP7-2 cells with imatinib or nilotinib (5 microM) also significantly inhibited the efflux of paclitaxel.
Imatinib and nilotinib reverse MRP7-mediated paclitaxel resistance, most likely due to their inhibition of the efflux of paclitaxel via MRP7. These findings suggest that imatinib or nilotinib, in combination with other antineoplastic drugs, may be useful in the treatment of certain resistant cancers.</description><subject>Abl protein</subject><subject>Antineoplastic agents</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Antineoplastic drugs</subject><subject>BCR protein</subject><subject>BCR-ABL protein</subject><subject>Benzamides</subject><subject>Binding sites</subject><subject>Cancer</subject><subject>Cancer cells</subject><subject>Cancer therapies</subject><subject>Cell Line</subject><subject>Chemotherapy</subject><subject>Competition</subject><subject>Cytotoxicity</subject><subject>Dermatology</subject><subject>Dose-Response Relationship, Drug</subject><subject>Drug resistance</subject><subject>Drug Resistance, Multiple</subject><subject>Drug Resistance, Neoplasm</subject><subject>Drugs</subject><subject>Efflux</subject><subject>Fusion protein</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Humans</subject><subject>Imatinib</subject><subject>Imatinib Mesylate</subject><subject>Inhibitor drugs</subject><subject>Kinases</subject><subject>Laboratories</subject><subject>Leukemia</subject><subject>Microbial drug resistance</subject><subject>Models, Chemical</subject><subject>Multidrug resistance</subject><subject>Multidrug Resistance-Associated Proteins - genetics</subject><subject>Multidrug Resistance-Associated Proteins - metabolism</subject><subject>Multidrug resistant organisms</subject><subject>Neoplasms - drug therapy</subject><subject>Neoplasms - metabolism</subject><subject>Paclitaxel</subject><subject>Paclitaxel - pharmacology</subject><subject>Pharmaceutical sciences</subject><subject>Pharmacology/Drug Development</subject><subject>Pharmacology/Drug Interactions</subject><subject>Pharmacology/Drug Resistance</subject><subject>Pharmacy</subject><subject>Piperazines - pharmacology</subject><subject>Protein-tyrosine kinase</subject><subject>Proteins</subject><subject>Pyrimidines - pharmacology</subject><subject>Sensitivity enhancement</subject><subject>Stem cells</subject><subject>Targeted cancer therapy</subject><subject>Tetrazolium Salts - pharmacology</subject><subject>Thiazoles - pharmacology</subject><subject>Tyrosine</subject><subject>Vincristine</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</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>eNqNkkuP0zAUhSMEYoaBf4AgEhJiFi2On8kGqVQ8Kg0aNDy2luNcp67SuNhONeXX404DtAsklEWck--c3FydLHtaoGlBRPF65Qbfq266cT1MEUKCYXQvOy8qgiccI3L_6HyWPQphhRAjJecPs7OiKmkhSHWe_VysVbS9rXPVN3lvO3d48rAFHyBfD120jR_apAQbouo15LbP9f7gcw1dF_J6l6SlrW3ytnlcQg7GdMNtrnS0Wxt3uTN38qebzyJ_NXs7nxfo8nH2wKguwJPxfpF9e__u6_zj5Or6w2I-u5pozkmcmKLWnHBKBG6axgAW3BgiKiKAaaBM47KqlWmQgbIUzDSUlUIDGE0YQiUlF9nzQ-6mc0GOawuywBWmvCz4nlgciMapldx4u1Z-J52y8k5wvpXKR6s7kEwoRrGggJWhRNclB8bTELrWgrOyTllvxq8N9RoaDX30qjsJPX3T26Vs3VZiwSqGWQp4MQZ492OAEP8x8vRAtSpNZXvjUphOVwNrq1MljE36jApcUkxJlQyXJ4bERLiNrRpCkIsvN__PXn8_ZV8esUtQXVwG1w3Ruj6cgvQAau9C8GD-7KRAct_o3_8p942WY6OT7dnxPv-axgqTXweI8po</recordid><startdate>20091020</startdate><enddate>20091020</enddate><creator>Shen, Tong</creator><creator>Kuang, Ye-Hong</creator><creator>Ashby, Charles R</creator><creator>Lei, Yu</creator><creator>Chen, Angel</creator><creator>Zhou, Ying</creator><creator>Chen, Xiang</creator><creator>Tiwari, Amit K</creator><creator>Hopper-Borge, Elizabeth</creator><creator>Ouyang, Jiangyong</creator><creator>Chen, Zhe-Sheng</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>IOV</scope><scope>ISR</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>AEUYN</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>5PM</scope><scope>DOA</scope></search><sort><creationdate>20091020</creationdate><title>Imatinib and nilotinib reverse multidrug resistance in cancer cells by inhibiting the efflux activity of the MRP7 (ABCC10)</title><author>Shen, Tong ; Kuang, Ye-Hong ; Ashby, Charles R ; Lei, Yu ; Chen, Angel ; Zhou, Ying ; Chen, Xiang ; Tiwari, Amit K ; Hopper-Borge, Elizabeth ; Ouyang, Jiangyong ; Chen, Zhe-Sheng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c663t-f1bc6364372dddfe276ff37937e5ce45c289bafd0fe8875fd4587ceefc3500843</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Abl protein</topic><topic>Antineoplastic agents</topic><topic>Antineoplastic Agents - pharmacology</topic><topic>Antineoplastic drugs</topic><topic>BCR protein</topic><topic>BCR-ABL protein</topic><topic>Benzamides</topic><topic>Binding sites</topic><topic>Cancer</topic><topic>Cancer cells</topic><topic>Cancer therapies</topic><topic>Cell Line</topic><topic>Chemotherapy</topic><topic>Competition</topic><topic>Cytotoxicity</topic><topic>Dermatology</topic><topic>Dose-Response Relationship, Drug</topic><topic>Drug resistance</topic><topic>Drug Resistance, Multiple</topic><topic>Drug Resistance, Neoplasm</topic><topic>Drugs</topic><topic>Efflux</topic><topic>Fusion protein</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Humans</topic><topic>Imatinib</topic><topic>Imatinib Mesylate</topic><topic>Inhibitor drugs</topic><topic>Kinases</topic><topic>Laboratories</topic><topic>Leukemia</topic><topic>Microbial drug resistance</topic><topic>Models, Chemical</topic><topic>Multidrug resistance</topic><topic>Multidrug Resistance-Associated Proteins - genetics</topic><topic>Multidrug Resistance-Associated Proteins - metabolism</topic><topic>Multidrug resistant organisms</topic><topic>Neoplasms - drug therapy</topic><topic>Neoplasms - metabolism</topic><topic>Paclitaxel</topic><topic>Paclitaxel - pharmacology</topic><topic>Pharmaceutical sciences</topic><topic>Pharmacology/Drug Development</topic><topic>Pharmacology/Drug Interactions</topic><topic>Pharmacology/Drug Resistance</topic><topic>Pharmacy</topic><topic>Piperazines - pharmacology</topic><topic>Protein-tyrosine kinase</topic><topic>Proteins</topic><topic>Pyrimidines - pharmacology</topic><topic>Sensitivity enhancement</topic><topic>Stem cells</topic><topic>Targeted cancer therapy</topic><topic>Tetrazolium Salts - pharmacology</topic><topic>Thiazoles - pharmacology</topic><topic>Tyrosine</topic><topic>Vincristine</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shen, Tong</creatorcontrib><creatorcontrib>Kuang, Ye-Hong</creatorcontrib><creatorcontrib>Ashby, Charles R</creatorcontrib><creatorcontrib>Lei, Yu</creatorcontrib><creatorcontrib>Chen, Angel</creatorcontrib><creatorcontrib>Zhou, Ying</creatorcontrib><creatorcontrib>Chen, Xiang</creatorcontrib><creatorcontrib>Tiwari, Amit K</creatorcontrib><creatorcontrib>Hopper-Borge, Elizabeth</creatorcontrib><creatorcontrib>Ouyang, Jiangyong</creatorcontrib><creatorcontrib>Chen, Zhe-Sheng</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</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 One Sustainability</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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The ABC transporters can significantly decrease the intracellular concentration of antineoplastic drugs by increasing their efflux, thereby lowering the cytotoxic activity of antineoplastic drugs. One of these transporters, the multiple resistant protein 7 (MRP7, ABCC10), has recently been shown to produce resistance to antineoplastic drugs by increasing the efflux of paclitaxel. In this study, we examined the effects of BCR-Abl tyrosine kinase inhibitors imatinib, nilotinib and dasatinib on the activity and expression of MRP7 in HEK293 cells transfected with MRP7, designated HEK-MRP7-2.
We report for the first time that imatinib and nilotinib reversed MRP7-mediated multidrug resistance. Our MTT assay results indicated that MRP7 expression in HEK-MRP7-2 cells was not significantly altered by incubation with 5 microM of imatinib or nilotinib for up to 72 hours. In addition, imatinib and nilotinib (1-5 microM) produced a significant concentration-dependent reversal of MRP7-mediated multidrug resistance by enhancing the sensitivity of HEK-MRP7-2 cells to paclitaxel and vincristine. Imatinib and nilotinib, at 5 microM, significantly increased the accumulation of [(3)H]-paclitaxel in HEK-MRP7-2 cells. The incubation of the HEK-MRP7-2 cells with imatinib or nilotinib (5 microM) also significantly inhibited the efflux of paclitaxel.
Imatinib and nilotinib reverse MRP7-mediated paclitaxel resistance, most likely due to their inhibition of the efflux of paclitaxel via MRP7. These findings suggest that imatinib or nilotinib, in combination with other antineoplastic drugs, may be useful in the treatment of certain resistant cancers.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>19841739</pmid><doi>10.1371/journal.pone.0007520</doi><tpages>e7520</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2009-10, Vol.4 (10), p.e7520 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1292468164 |
| 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 | Abl protein Antineoplastic agents Antineoplastic Agents - pharmacology Antineoplastic drugs BCR protein BCR-ABL protein Benzamides Binding sites Cancer Cancer cells Cancer therapies Cell Line Chemotherapy Competition Cytotoxicity Dermatology Dose-Response Relationship, Drug Drug resistance Drug Resistance, Multiple Drug Resistance, Neoplasm Drugs Efflux Fusion protein Gene Expression Regulation, Neoplastic Humans Imatinib Imatinib Mesylate Inhibitor drugs Kinases Laboratories Leukemia Microbial drug resistance Models, Chemical Multidrug resistance Multidrug Resistance-Associated Proteins - genetics Multidrug Resistance-Associated Proteins - metabolism Multidrug resistant organisms Neoplasms - drug therapy Neoplasms - metabolism Paclitaxel Paclitaxel - pharmacology Pharmaceutical sciences Pharmacology/Drug Development Pharmacology/Drug Interactions Pharmacology/Drug Resistance Pharmacy Piperazines - pharmacology Protein-tyrosine kinase Proteins Pyrimidines - pharmacology Sensitivity enhancement Stem cells Targeted cancer therapy Tetrazolium Salts - pharmacology Thiazoles - pharmacology Tyrosine Vincristine |
| title | Imatinib and nilotinib reverse multidrug resistance in cancer cells by inhibiting the efflux activity of the MRP7 (ABCC10) |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-11T16%3A12%3A47IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Imatinib%20and%20nilotinib%20reverse%20multidrug%20resistance%20in%20cancer%20cells%20by%20inhibiting%20the%20efflux%20activity%20of%20the%20MRP7%20(ABCC10)&rft.jtitle=PloS%20one&rft.au=Shen,%20Tong&rft.date=2009-10-20&rft.volume=4&rft.issue=10&rft.spage=e7520&rft.pages=e7520-&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0007520&rft_dat=%3Cgale_plos_%3EA472842439%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1292468164&rft_id=info:pmid/19841739&rft_galeid=A472842439&rft_doaj_id=oai_doaj_org_article_57a54274e2af43cb86e5645ccbc7658b&rfr_iscdi=true |