HSA-based multi-target combination therapy: regulating drugs’ release from HSA and overcoming single drug resistance in a breast cancer model
Multi-drug delivery systems, which may be promising solution to overcome obstacles, have limited the clinical success of multi-drug combination therapies to treat cancer. To this end, we used three different anticancer agents, Cu(BpT)Br, NAMI-A, and doxorubicin (DOX), to build human serum albumin (H...
Ausführliche Beschreibung
Autor*in: |
Yi Gou [verfasserIn] Zhenlei Zhang [verfasserIn] Dongyang Li [verfasserIn] Lei Zhao [verfasserIn] Meiling Cai [verfasserIn] Zhewen Sun [verfasserIn] Yongping Li [verfasserIn] Yao Zhang [verfasserIn] Hamid Khan [verfasserIn] Hongbing Sun [verfasserIn] Tao Wang [verfasserIn] Hong Liang [verfasserIn] Feng Yang [verfasserIn] |
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E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2018 |
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Übergeordnetes Werk: |
In: Drug Delivery - Taylor & Francis Group, 2017, 25(2018), 1, Seite 321-329 |
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Übergeordnetes Werk: |
volume:25 ; year:2018 ; number:1 ; pages:321-329 |
Links: |
Link aufrufen |
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DOI / URN: |
10.1080/10717544.2018.1428245 |
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Katalog-ID: |
DOAJ032732015 |
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10.1080/10717544.2018.1428245 doi (DE-627)DOAJ032732015 (DE-599)DOAJa48e3334db4941ed9fa2060fdd9aff3d DE-627 ger DE-627 rakwb eng RM1-950 Yi Gou verfasserin aut HSA-based multi-target combination therapy: regulating drugs’ release from HSA and overcoming single drug resistance in a breast cancer model 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Multi-drug delivery systems, which may be promising solution to overcome obstacles, have limited the clinical success of multi-drug combination therapies to treat cancer. To this end, we used three different anticancer agents, Cu(BpT)Br, NAMI-A, and doxorubicin (DOX), to build human serum albumin (HSA)-based multi-drug delivery systems in a breast cancer model to investigate the therapeutic efficacy of overcoming single drug (DOX) resistance to cancer cells in vivo, and to regulate the drugs’ release from HSA. The HSA complex structure revealed that NAMI-A and Cu(BpT)Br bind to the IB and IIA sub-domain of HSA by N-donor residue replacing a leaving group and coordinating to their metal centers, respectively. The MALDI-TOF mass spectra demonstrated that one DOX molecule is conjugated with lysine of HSA by a pH-sensitive linker. Furthermore, the release behavior of three agents form HSA can be regulated at different pH levels. Importantly, in vivo results revealed that the HSA–NAMI-A–Cu(BpT)Br–DOX complex not only increases the targeting ability compared with a combination of the three agents (the NAMI-A/Cu(BpT)Br/DOX mixture), but it also overcomes DOX resistance to drug-resistant breast cancer cell lines. albumin combination therapy drug delivery systems drug release drug resistant Therapeutics. Pharmacology Zhenlei Zhang verfasserin aut Dongyang Li verfasserin aut Lei Zhao verfasserin aut Meiling Cai verfasserin aut Zhewen Sun verfasserin aut Yongping Li verfasserin aut Yao Zhang verfasserin aut Hamid Khan verfasserin aut Hongbing Sun verfasserin aut Tao Wang verfasserin aut Hong Liang verfasserin aut Feng Yang verfasserin aut In Drug Delivery Taylor & Francis Group, 2017 25(2018), 1, Seite 321-329 (DE-627)320604675 (DE-600)2020593-4 15210464 nnns volume:25 year:2018 number:1 pages:321-329 https://doi.org/10.1080/10717544.2018.1428245 kostenfrei https://doaj.org/article/a48e3334db4941ed9fa2060fdd9aff3d kostenfrei http://dx.doi.org/10.1080/10717544.2018.1428245 kostenfrei https://doaj.org/toc/1071-7544 Journal toc kostenfrei https://doaj.org/toc/1521-0464 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_1200 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 25 2018 1 321-329 |
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10.1080/10717544.2018.1428245 doi (DE-627)DOAJ032732015 (DE-599)DOAJa48e3334db4941ed9fa2060fdd9aff3d DE-627 ger DE-627 rakwb eng RM1-950 Yi Gou verfasserin aut HSA-based multi-target combination therapy: regulating drugs’ release from HSA and overcoming single drug resistance in a breast cancer model 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Multi-drug delivery systems, which may be promising solution to overcome obstacles, have limited the clinical success of multi-drug combination therapies to treat cancer. To this end, we used three different anticancer agents, Cu(BpT)Br, NAMI-A, and doxorubicin (DOX), to build human serum albumin (HSA)-based multi-drug delivery systems in a breast cancer model to investigate the therapeutic efficacy of overcoming single drug (DOX) resistance to cancer cells in vivo, and to regulate the drugs’ release from HSA. The HSA complex structure revealed that NAMI-A and Cu(BpT)Br bind to the IB and IIA sub-domain of HSA by N-donor residue replacing a leaving group and coordinating to their metal centers, respectively. The MALDI-TOF mass spectra demonstrated that one DOX molecule is conjugated with lysine of HSA by a pH-sensitive linker. Furthermore, the release behavior of three agents form HSA can be regulated at different pH levels. Importantly, in vivo results revealed that the HSA–NAMI-A–Cu(BpT)Br–DOX complex not only increases the targeting ability compared with a combination of the three agents (the NAMI-A/Cu(BpT)Br/DOX mixture), but it also overcomes DOX resistance to drug-resistant breast cancer cell lines. albumin combination therapy drug delivery systems drug release drug resistant Therapeutics. Pharmacology Zhenlei Zhang verfasserin aut Dongyang Li verfasserin aut Lei Zhao verfasserin aut Meiling Cai verfasserin aut Zhewen Sun verfasserin aut Yongping Li verfasserin aut Yao Zhang verfasserin aut Hamid Khan verfasserin aut Hongbing Sun verfasserin aut Tao Wang verfasserin aut Hong Liang verfasserin aut Feng Yang verfasserin aut In Drug Delivery Taylor & Francis Group, 2017 25(2018), 1, Seite 321-329 (DE-627)320604675 (DE-600)2020593-4 15210464 nnns volume:25 year:2018 number:1 pages:321-329 https://doi.org/10.1080/10717544.2018.1428245 kostenfrei https://doaj.org/article/a48e3334db4941ed9fa2060fdd9aff3d kostenfrei http://dx.doi.org/10.1080/10717544.2018.1428245 kostenfrei https://doaj.org/toc/1071-7544 Journal toc kostenfrei https://doaj.org/toc/1521-0464 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_1200 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 25 2018 1 321-329 |
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10.1080/10717544.2018.1428245 doi (DE-627)DOAJ032732015 (DE-599)DOAJa48e3334db4941ed9fa2060fdd9aff3d DE-627 ger DE-627 rakwb eng RM1-950 Yi Gou verfasserin aut HSA-based multi-target combination therapy: regulating drugs’ release from HSA and overcoming single drug resistance in a breast cancer model 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Multi-drug delivery systems, which may be promising solution to overcome obstacles, have limited the clinical success of multi-drug combination therapies to treat cancer. To this end, we used three different anticancer agents, Cu(BpT)Br, NAMI-A, and doxorubicin (DOX), to build human serum albumin (HSA)-based multi-drug delivery systems in a breast cancer model to investigate the therapeutic efficacy of overcoming single drug (DOX) resistance to cancer cells in vivo, and to regulate the drugs’ release from HSA. The HSA complex structure revealed that NAMI-A and Cu(BpT)Br bind to the IB and IIA sub-domain of HSA by N-donor residue replacing a leaving group and coordinating to their metal centers, respectively. The MALDI-TOF mass spectra demonstrated that one DOX molecule is conjugated with lysine of HSA by a pH-sensitive linker. Furthermore, the release behavior of three agents form HSA can be regulated at different pH levels. Importantly, in vivo results revealed that the HSA–NAMI-A–Cu(BpT)Br–DOX complex not only increases the targeting ability compared with a combination of the three agents (the NAMI-A/Cu(BpT)Br/DOX mixture), but it also overcomes DOX resistance to drug-resistant breast cancer cell lines. albumin combination therapy drug delivery systems drug release drug resistant Therapeutics. Pharmacology Zhenlei Zhang verfasserin aut Dongyang Li verfasserin aut Lei Zhao verfasserin aut Meiling Cai verfasserin aut Zhewen Sun verfasserin aut Yongping Li verfasserin aut Yao Zhang verfasserin aut Hamid Khan verfasserin aut Hongbing Sun verfasserin aut Tao Wang verfasserin aut Hong Liang verfasserin aut Feng Yang verfasserin aut In Drug Delivery Taylor & Francis Group, 2017 25(2018), 1, Seite 321-329 (DE-627)320604675 (DE-600)2020593-4 15210464 nnns volume:25 year:2018 number:1 pages:321-329 https://doi.org/10.1080/10717544.2018.1428245 kostenfrei https://doaj.org/article/a48e3334db4941ed9fa2060fdd9aff3d kostenfrei http://dx.doi.org/10.1080/10717544.2018.1428245 kostenfrei https://doaj.org/toc/1071-7544 Journal toc kostenfrei https://doaj.org/toc/1521-0464 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_1200 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 25 2018 1 321-329 |
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10.1080/10717544.2018.1428245 doi (DE-627)DOAJ032732015 (DE-599)DOAJa48e3334db4941ed9fa2060fdd9aff3d DE-627 ger DE-627 rakwb eng RM1-950 Yi Gou verfasserin aut HSA-based multi-target combination therapy: regulating drugs’ release from HSA and overcoming single drug resistance in a breast cancer model 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Multi-drug delivery systems, which may be promising solution to overcome obstacles, have limited the clinical success of multi-drug combination therapies to treat cancer. To this end, we used three different anticancer agents, Cu(BpT)Br, NAMI-A, and doxorubicin (DOX), to build human serum albumin (HSA)-based multi-drug delivery systems in a breast cancer model to investigate the therapeutic efficacy of overcoming single drug (DOX) resistance to cancer cells in vivo, and to regulate the drugs’ release from HSA. The HSA complex structure revealed that NAMI-A and Cu(BpT)Br bind to the IB and IIA sub-domain of HSA by N-donor residue replacing a leaving group and coordinating to their metal centers, respectively. The MALDI-TOF mass spectra demonstrated that one DOX molecule is conjugated with lysine of HSA by a pH-sensitive linker. Furthermore, the release behavior of three agents form HSA can be regulated at different pH levels. Importantly, in vivo results revealed that the HSA–NAMI-A–Cu(BpT)Br–DOX complex not only increases the targeting ability compared with a combination of the three agents (the NAMI-A/Cu(BpT)Br/DOX mixture), but it also overcomes DOX resistance to drug-resistant breast cancer cell lines. albumin combination therapy drug delivery systems drug release drug resistant Therapeutics. Pharmacology Zhenlei Zhang verfasserin aut Dongyang Li verfasserin aut Lei Zhao verfasserin aut Meiling Cai verfasserin aut Zhewen Sun verfasserin aut Yongping Li verfasserin aut Yao Zhang verfasserin aut Hamid Khan verfasserin aut Hongbing Sun verfasserin aut Tao Wang verfasserin aut Hong Liang verfasserin aut Feng Yang verfasserin aut In Drug Delivery Taylor & Francis Group, 2017 25(2018), 1, Seite 321-329 (DE-627)320604675 (DE-600)2020593-4 15210464 nnns volume:25 year:2018 number:1 pages:321-329 https://doi.org/10.1080/10717544.2018.1428245 kostenfrei https://doaj.org/article/a48e3334db4941ed9fa2060fdd9aff3d kostenfrei http://dx.doi.org/10.1080/10717544.2018.1428245 kostenfrei https://doaj.org/toc/1071-7544 Journal toc kostenfrei https://doaj.org/toc/1521-0464 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_1200 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 25 2018 1 321-329 |
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10.1080/10717544.2018.1428245 doi (DE-627)DOAJ032732015 (DE-599)DOAJa48e3334db4941ed9fa2060fdd9aff3d DE-627 ger DE-627 rakwb eng RM1-950 Yi Gou verfasserin aut HSA-based multi-target combination therapy: regulating drugs’ release from HSA and overcoming single drug resistance in a breast cancer model 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Multi-drug delivery systems, which may be promising solution to overcome obstacles, have limited the clinical success of multi-drug combination therapies to treat cancer. To this end, we used three different anticancer agents, Cu(BpT)Br, NAMI-A, and doxorubicin (DOX), to build human serum albumin (HSA)-based multi-drug delivery systems in a breast cancer model to investigate the therapeutic efficacy of overcoming single drug (DOX) resistance to cancer cells in vivo, and to regulate the drugs’ release from HSA. The HSA complex structure revealed that NAMI-A and Cu(BpT)Br bind to the IB and IIA sub-domain of HSA by N-donor residue replacing a leaving group and coordinating to their metal centers, respectively. The MALDI-TOF mass spectra demonstrated that one DOX molecule is conjugated with lysine of HSA by a pH-sensitive linker. Furthermore, the release behavior of three agents form HSA can be regulated at different pH levels. Importantly, in vivo results revealed that the HSA–NAMI-A–Cu(BpT)Br–DOX complex not only increases the targeting ability compared with a combination of the three agents (the NAMI-A/Cu(BpT)Br/DOX mixture), but it also overcomes DOX resistance to drug-resistant breast cancer cell lines. albumin combination therapy drug delivery systems drug release drug resistant Therapeutics. Pharmacology Zhenlei Zhang verfasserin aut Dongyang Li verfasserin aut Lei Zhao verfasserin aut Meiling Cai verfasserin aut Zhewen Sun verfasserin aut Yongping Li verfasserin aut Yao Zhang verfasserin aut Hamid Khan verfasserin aut Hongbing Sun verfasserin aut Tao Wang verfasserin aut Hong Liang verfasserin aut Feng Yang verfasserin aut In Drug Delivery Taylor & Francis Group, 2017 25(2018), 1, Seite 321-329 (DE-627)320604675 (DE-600)2020593-4 15210464 nnns volume:25 year:2018 number:1 pages:321-329 https://doi.org/10.1080/10717544.2018.1428245 kostenfrei https://doaj.org/article/a48e3334db4941ed9fa2060fdd9aff3d kostenfrei http://dx.doi.org/10.1080/10717544.2018.1428245 kostenfrei https://doaj.org/toc/1071-7544 Journal toc kostenfrei https://doaj.org/toc/1521-0464 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_1200 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 25 2018 1 321-329 |
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Yi Gou Zhenlei Zhang Dongyang Li Lei Zhao Meiling Cai Zhewen Sun Yongping Li Yao Zhang Hamid Khan Hongbing Sun Tao Wang Hong Liang Feng Yang |
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HSA-based multi-target combination therapy: regulating drugs’ release from HSA and overcoming single drug resistance in a breast cancer model |
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Multi-drug delivery systems, which may be promising solution to overcome obstacles, have limited the clinical success of multi-drug combination therapies to treat cancer. To this end, we used three different anticancer agents, Cu(BpT)Br, NAMI-A, and doxorubicin (DOX), to build human serum albumin (HSA)-based multi-drug delivery systems in a breast cancer model to investigate the therapeutic efficacy of overcoming single drug (DOX) resistance to cancer cells in vivo, and to regulate the drugs’ release from HSA. The HSA complex structure revealed that NAMI-A and Cu(BpT)Br bind to the IB and IIA sub-domain of HSA by N-donor residue replacing a leaving group and coordinating to their metal centers, respectively. The MALDI-TOF mass spectra demonstrated that one DOX molecule is conjugated with lysine of HSA by a pH-sensitive linker. Furthermore, the release behavior of three agents form HSA can be regulated at different pH levels. Importantly, in vivo results revealed that the HSA–NAMI-A–Cu(BpT)Br–DOX complex not only increases the targeting ability compared with a combination of the three agents (the NAMI-A/Cu(BpT)Br/DOX mixture), but it also overcomes DOX resistance to drug-resistant breast cancer cell lines. |
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Multi-drug delivery systems, which may be promising solution to overcome obstacles, have limited the clinical success of multi-drug combination therapies to treat cancer. To this end, we used three different anticancer agents, Cu(BpT)Br, NAMI-A, and doxorubicin (DOX), to build human serum albumin (HSA)-based multi-drug delivery systems in a breast cancer model to investigate the therapeutic efficacy of overcoming single drug (DOX) resistance to cancer cells in vivo, and to regulate the drugs’ release from HSA. The HSA complex structure revealed that NAMI-A and Cu(BpT)Br bind to the IB and IIA sub-domain of HSA by N-donor residue replacing a leaving group and coordinating to their metal centers, respectively. The MALDI-TOF mass spectra demonstrated that one DOX molecule is conjugated with lysine of HSA by a pH-sensitive linker. Furthermore, the release behavior of three agents form HSA can be regulated at different pH levels. Importantly, in vivo results revealed that the HSA–NAMI-A–Cu(BpT)Br–DOX complex not only increases the targeting ability compared with a combination of the three agents (the NAMI-A/Cu(BpT)Br/DOX mixture), but it also overcomes DOX resistance to drug-resistant breast cancer cell lines. |
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Multi-drug delivery systems, which may be promising solution to overcome obstacles, have limited the clinical success of multi-drug combination therapies to treat cancer. To this end, we used three different anticancer agents, Cu(BpT)Br, NAMI-A, and doxorubicin (DOX), to build human serum albumin (HSA)-based multi-drug delivery systems in a breast cancer model to investigate the therapeutic efficacy of overcoming single drug (DOX) resistance to cancer cells in vivo, and to regulate the drugs’ release from HSA. The HSA complex structure revealed that NAMI-A and Cu(BpT)Br bind to the IB and IIA sub-domain of HSA by N-donor residue replacing a leaving group and coordinating to their metal centers, respectively. The MALDI-TOF mass spectra demonstrated that one DOX molecule is conjugated with lysine of HSA by a pH-sensitive linker. Furthermore, the release behavior of three agents form HSA can be regulated at different pH levels. Importantly, in vivo results revealed that the HSA–NAMI-A–Cu(BpT)Br–DOX complex not only increases the targeting ability compared with a combination of the three agents (the NAMI-A/Cu(BpT)Br/DOX mixture), but it also overcomes DOX resistance to drug-resistant breast cancer cell lines. |
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