Decitabine/paclitaxel co-delivery systems modified with anti-PD-L1 antibodies mediate chemoimmunotherapy for Triple negative breast cancer
Triple-negative breast cancer (TNBC) is one of the major clinical problems to be solved urgently, because of its high malignancy, poor targeted therapy effect and easy occurrence of drug resistance and metastasis. Here, methyltransferase DNMT1 was identified as a key factor mediating PTX resistance...
Ausführliche Beschreibung
Autor*in: |
Yang He [verfasserIn] Qin Hu [verfasserIn] Liting Wang [verfasserIn] Chuanrong Chen [verfasserIn] |
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E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2024 |
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Übergeordnetes Werk: |
In: Materials & Design - Elsevier, 2019, 237(2024), Seite 112562- |
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Übergeordnetes Werk: |
volume:237 ; year:2024 ; pages:112562- |
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DOI / URN: |
10.1016/j.matdes.2023.112562 |
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Katalog-ID: |
DOAJ096525045 |
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520 | |a Triple-negative breast cancer (TNBC) is one of the major clinical problems to be solved urgently, because of its high malignancy, poor targeted therapy effect and easy occurrence of drug resistance and metastasis. Here, methyltransferase DNMT1 was identified as a key factor mediating PTX resistance for TNBC. Decitabine (DEC), an inhibitor of DNMT1, can inhibit the proliferation and metastasis of TNBC cells and reverse PTX resistance. In this study, we reported a new delivery system (DEC/PTX NPsαPD-L1) co-loaded with DEC and PTX modified by anti-PD-L1 monoclonal antibody (αPD-L1), which can overcome drug resistance and metastasis through multi-mode synergistic effect. αPD-L1 increases the enrichment of nanoparticles in tumor tissue through active targeting effect, and blocks PD-L1 on the surface of TNBC cells, thereby activating anti-tumor immune while enhancing internalization of nanoparticles by tumor cells. Inside tumor cells, DEC inhibits EMT process and cancer stem cells to overcome PTX resistance and metastasis. PTX can not only exerts direct tumor killing effect, but also inhibit Treg cells from remodeling immune microenvironment, and induces efficient immunogenic death in cooperation with DEC. This delivery system, realizing tumor-specific synchronized chemoimmunotherapy, represents a promising therapeutic platform for TNBC. | ||
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10.1016/j.matdes.2023.112562 doi (DE-627)DOAJ096525045 (DE-599)DOAJ545fcd8f3ad84253aa856cc228830ee1 DE-627 ger DE-627 rakwb eng TA401-492 Yang He verfasserin aut Decitabine/paclitaxel co-delivery systems modified with anti-PD-L1 antibodies mediate chemoimmunotherapy for Triple negative breast cancer 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Triple-negative breast cancer (TNBC) is one of the major clinical problems to be solved urgently, because of its high malignancy, poor targeted therapy effect and easy occurrence of drug resistance and metastasis. Here, methyltransferase DNMT1 was identified as a key factor mediating PTX resistance for TNBC. Decitabine (DEC), an inhibitor of DNMT1, can inhibit the proliferation and metastasis of TNBC cells and reverse PTX resistance. In this study, we reported a new delivery system (DEC/PTX NPsαPD-L1) co-loaded with DEC and PTX modified by anti-PD-L1 monoclonal antibody (αPD-L1), which can overcome drug resistance and metastasis through multi-mode synergistic effect. αPD-L1 increases the enrichment of nanoparticles in tumor tissue through active targeting effect, and blocks PD-L1 on the surface of TNBC cells, thereby activating anti-tumor immune while enhancing internalization of nanoparticles by tumor cells. Inside tumor cells, DEC inhibits EMT process and cancer stem cells to overcome PTX resistance and metastasis. PTX can not only exerts direct tumor killing effect, but also inhibit Treg cells from remodeling immune microenvironment, and induces efficient immunogenic death in cooperation with DEC. This delivery system, realizing tumor-specific synchronized chemoimmunotherapy, represents a promising therapeutic platform for TNBC. DNMT1 Immunotherapy PD-L1 Co-delivery Immunogenic cell death Materials of engineering and construction. Mechanics of materials Qin Hu verfasserin aut Liting Wang verfasserin aut Chuanrong Chen verfasserin aut In Materials & Design Elsevier, 2019 237(2024), Seite 112562- (DE-627)32052857X (DE-600)2015480-X 18734197 nnns volume:237 year:2024 pages:112562- https://doi.org/10.1016/j.matdes.2023.112562 kostenfrei https://doaj.org/article/545fcd8f3ad84253aa856cc228830ee1 kostenfrei http://www.sciencedirect.com/science/article/pii/S0264127523009784 kostenfrei https://doaj.org/toc/0264-1275 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 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_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2007 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_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 237 2024 112562- |
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10.1016/j.matdes.2023.112562 doi (DE-627)DOAJ096525045 (DE-599)DOAJ545fcd8f3ad84253aa856cc228830ee1 DE-627 ger DE-627 rakwb eng TA401-492 Yang He verfasserin aut Decitabine/paclitaxel co-delivery systems modified with anti-PD-L1 antibodies mediate chemoimmunotherapy for Triple negative breast cancer 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Triple-negative breast cancer (TNBC) is one of the major clinical problems to be solved urgently, because of its high malignancy, poor targeted therapy effect and easy occurrence of drug resistance and metastasis. Here, methyltransferase DNMT1 was identified as a key factor mediating PTX resistance for TNBC. Decitabine (DEC), an inhibitor of DNMT1, can inhibit the proliferation and metastasis of TNBC cells and reverse PTX resistance. In this study, we reported a new delivery system (DEC/PTX NPsαPD-L1) co-loaded with DEC and PTX modified by anti-PD-L1 monoclonal antibody (αPD-L1), which can overcome drug resistance and metastasis through multi-mode synergistic effect. αPD-L1 increases the enrichment of nanoparticles in tumor tissue through active targeting effect, and blocks PD-L1 on the surface of TNBC cells, thereby activating anti-tumor immune while enhancing internalization of nanoparticles by tumor cells. Inside tumor cells, DEC inhibits EMT process and cancer stem cells to overcome PTX resistance and metastasis. PTX can not only exerts direct tumor killing effect, but also inhibit Treg cells from remodeling immune microenvironment, and induces efficient immunogenic death in cooperation with DEC. This delivery system, realizing tumor-specific synchronized chemoimmunotherapy, represents a promising therapeutic platform for TNBC. DNMT1 Immunotherapy PD-L1 Co-delivery Immunogenic cell death Materials of engineering and construction. Mechanics of materials Qin Hu verfasserin aut Liting Wang verfasserin aut Chuanrong Chen verfasserin aut In Materials & Design Elsevier, 2019 237(2024), Seite 112562- (DE-627)32052857X (DE-600)2015480-X 18734197 nnns volume:237 year:2024 pages:112562- https://doi.org/10.1016/j.matdes.2023.112562 kostenfrei https://doaj.org/article/545fcd8f3ad84253aa856cc228830ee1 kostenfrei http://www.sciencedirect.com/science/article/pii/S0264127523009784 kostenfrei https://doaj.org/toc/0264-1275 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 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_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2007 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_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 237 2024 112562- |
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Yang He misc TA401-492 misc DNMT1 misc Immunotherapy misc PD-L1 misc Co-delivery misc Immunogenic cell death misc Materials of engineering and construction. Mechanics of materials Decitabine/paclitaxel co-delivery systems modified with anti-PD-L1 antibodies mediate chemoimmunotherapy for Triple negative breast cancer |
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TA401-492 Decitabine/paclitaxel co-delivery systems modified with anti-PD-L1 antibodies mediate chemoimmunotherapy for Triple negative breast cancer DNMT1 Immunotherapy PD-L1 Co-delivery Immunogenic cell death |
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Decitabine/paclitaxel co-delivery systems modified with anti-PD-L1 antibodies mediate chemoimmunotherapy for Triple negative breast cancer |
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Decitabine/paclitaxel co-delivery systems modified with anti-PD-L1 antibodies mediate chemoimmunotherapy for Triple negative breast cancer |
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decitabine/paclitaxel co-delivery systems modified with anti-pd-l1 antibodies mediate chemoimmunotherapy for triple negative breast cancer |
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Decitabine/paclitaxel co-delivery systems modified with anti-PD-L1 antibodies mediate chemoimmunotherapy for Triple negative breast cancer |
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Triple-negative breast cancer (TNBC) is one of the major clinical problems to be solved urgently, because of its high malignancy, poor targeted therapy effect and easy occurrence of drug resistance and metastasis. Here, methyltransferase DNMT1 was identified as a key factor mediating PTX resistance for TNBC. Decitabine (DEC), an inhibitor of DNMT1, can inhibit the proliferation and metastasis of TNBC cells and reverse PTX resistance. In this study, we reported a new delivery system (DEC/PTX NPsαPD-L1) co-loaded with DEC and PTX modified by anti-PD-L1 monoclonal antibody (αPD-L1), which can overcome drug resistance and metastasis through multi-mode synergistic effect. αPD-L1 increases the enrichment of nanoparticles in tumor tissue through active targeting effect, and blocks PD-L1 on the surface of TNBC cells, thereby activating anti-tumor immune while enhancing internalization of nanoparticles by tumor cells. Inside tumor cells, DEC inhibits EMT process and cancer stem cells to overcome PTX resistance and metastasis. PTX can not only exerts direct tumor killing effect, but also inhibit Treg cells from remodeling immune microenvironment, and induces efficient immunogenic death in cooperation with DEC. This delivery system, realizing tumor-specific synchronized chemoimmunotherapy, represents a promising therapeutic platform for TNBC. |
abstractGer |
Triple-negative breast cancer (TNBC) is one of the major clinical problems to be solved urgently, because of its high malignancy, poor targeted therapy effect and easy occurrence of drug resistance and metastasis. Here, methyltransferase DNMT1 was identified as a key factor mediating PTX resistance for TNBC. Decitabine (DEC), an inhibitor of DNMT1, can inhibit the proliferation and metastasis of TNBC cells and reverse PTX resistance. In this study, we reported a new delivery system (DEC/PTX NPsαPD-L1) co-loaded with DEC and PTX modified by anti-PD-L1 monoclonal antibody (αPD-L1), which can overcome drug resistance and metastasis through multi-mode synergistic effect. αPD-L1 increases the enrichment of nanoparticles in tumor tissue through active targeting effect, and blocks PD-L1 on the surface of TNBC cells, thereby activating anti-tumor immune while enhancing internalization of nanoparticles by tumor cells. Inside tumor cells, DEC inhibits EMT process and cancer stem cells to overcome PTX resistance and metastasis. PTX can not only exerts direct tumor killing effect, but also inhibit Treg cells from remodeling immune microenvironment, and induces efficient immunogenic death in cooperation with DEC. This delivery system, realizing tumor-specific synchronized chemoimmunotherapy, represents a promising therapeutic platform for TNBC. |
abstract_unstemmed |
Triple-negative breast cancer (TNBC) is one of the major clinical problems to be solved urgently, because of its high malignancy, poor targeted therapy effect and easy occurrence of drug resistance and metastasis. Here, methyltransferase DNMT1 was identified as a key factor mediating PTX resistance for TNBC. Decitabine (DEC), an inhibitor of DNMT1, can inhibit the proliferation and metastasis of TNBC cells and reverse PTX resistance. In this study, we reported a new delivery system (DEC/PTX NPsαPD-L1) co-loaded with DEC and PTX modified by anti-PD-L1 monoclonal antibody (αPD-L1), which can overcome drug resistance and metastasis through multi-mode synergistic effect. αPD-L1 increases the enrichment of nanoparticles in tumor tissue through active targeting effect, and blocks PD-L1 on the surface of TNBC cells, thereby activating anti-tumor immune while enhancing internalization of nanoparticles by tumor cells. Inside tumor cells, DEC inhibits EMT process and cancer stem cells to overcome PTX resistance and metastasis. PTX can not only exerts direct tumor killing effect, but also inhibit Treg cells from remodeling immune microenvironment, and induces efficient immunogenic death in cooperation with DEC. This delivery system, realizing tumor-specific synchronized chemoimmunotherapy, represents a promising therapeutic platform for TNBC. |
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Decitabine/paclitaxel co-delivery systems modified with anti-PD-L1 antibodies mediate chemoimmunotherapy for Triple negative breast cancer |
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