Immunotherapy of Hepatocellular Carcinoma with Magnetic PD-1 Peptide-Imprinted Polymer Nanocomposite and Natural Killer Cells
Programmed cell death protein 1 (PD-1) is a biomarker on the surface of cells with a role in promoting self-tolerance by suppressing the inflammatory activity of T cells. In this work, one peptide of PD-1 was used as the template for molecular imprinting to form magnetic peptide-imprinted poly(ethyl...
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| Published in | Biomolecules (Basel, Switzerland) Vol. 9; no. 11; p. 651 |
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| Main Authors | , , , , |
| Format | Journal Article |
| Language | English |
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25.10.2019
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| Abstract | Programmed cell death protein 1 (PD-1) is a biomarker on the surface of cells with a role in promoting self-tolerance by suppressing the inflammatory activity of T cells. In this work, one peptide of PD-1 was used as the template for molecular imprinting to form magnetic peptide-imprinted poly(ethylene-co-vinyl alcohol) composite nanoparticles (MPIP NPs). The nanoparticles were characterized by dynamic light scattering (DLS), high-performance liquid chromatography (HPLC), Brunauer–Emmett–Teller (BET) analysis, and superconducting quantum interference device (SQUID) analysis. Natural killer 92 (NK-92) cells were added to these composite nanoparticles and then incubated with human hepatoma (HepG2) cells. The viability and the apoptosis pathway of HepG2 were then studied using cell counting kit-8 (CCK8) and quantitative real-time polymerase chain reaction (qRT-PCR), respectively. These nanoparticles were found to significantly enhance the activity of natural killer cells toward HepG2 cells by increasing the expression of nuclear factor kappa B (NF-κB), caspase 8, and especially caspase 3. |
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| AbstractList | Programmed cell death protein 1 (PD-1) is a biomarker on the surface of cells with a role in promoting self-tolerance by suppressing the inflammatory activity of T cells. In this work, one peptide of PD-1 was used as the template for molecular imprinting to form magnetic peptide-imprinted poly(ethylene-
-vinyl alcohol) composite nanoparticles (MPIP NPs). The nanoparticles were characterized by dynamic light scattering (DLS), high-performance liquid chromatography (HPLC), Brunauer-Emmett-Teller (BET) analysis, and superconducting quantum interference device (SQUID) analysis. Natural killer 92 (NK-92) cells were added to these composite nanoparticles and then incubated with human hepatoma (HepG2) cells. The viability and the apoptosis pathway of HepG2 were then studied using cell counting kit-8 (CCK8) and quantitative real-time polymerase chain reaction (qRT-PCR), respectively. These nanoparticles were found to significantly enhance the activity of natural killer cells toward HepG2 cells by increasing the expression of nuclear factor kappa B (NF-κB), caspase 8, and especially caspase 3. Programmed cell death protein 1 (PD-1) is a biomarker on the surface of cells with a role in promoting self-tolerance by suppressing the inflammatory activity of T cells. In this work, one peptide of PD-1 was used as the template for molecular imprinting to form magnetic peptide-imprinted poly(ethylene-co-vinyl alcohol) composite nanoparticles (MPIP NPs). The nanoparticles were characterized by dynamic light scattering (DLS), high-performance liquid chromatography (HPLC), Brunauer-Emmett-Teller (BET) analysis, and superconducting quantum interference device (SQUID) analysis. Natural killer 92 (NK-92) cells were added to these composite nanoparticles and then incubated with human hepatoma (HepG2) cells. The viability and the apoptosis pathway of HepG2 were then studied using cell counting kit-8 (CCK8) and quantitative real-time polymerase chain reaction (qRT-PCR), respectively. These nanoparticles were found to significantly enhance the activity of natural killer cells toward HepG2 cells by increasing the expression of nuclear factor kappa B (NF-κB), caspase 8, and especially caspase 3.Programmed cell death protein 1 (PD-1) is a biomarker on the surface of cells with a role in promoting self-tolerance by suppressing the inflammatory activity of T cells. In this work, one peptide of PD-1 was used as the template for molecular imprinting to form magnetic peptide-imprinted poly(ethylene-co-vinyl alcohol) composite nanoparticles (MPIP NPs). The nanoparticles were characterized by dynamic light scattering (DLS), high-performance liquid chromatography (HPLC), Brunauer-Emmett-Teller (BET) analysis, and superconducting quantum interference device (SQUID) analysis. Natural killer 92 (NK-92) cells were added to these composite nanoparticles and then incubated with human hepatoma (HepG2) cells. The viability and the apoptosis pathway of HepG2 were then studied using cell counting kit-8 (CCK8) and quantitative real-time polymerase chain reaction (qRT-PCR), respectively. These nanoparticles were found to significantly enhance the activity of natural killer cells toward HepG2 cells by increasing the expression of nuclear factor kappa B (NF-κB), caspase 8, and especially caspase 3. Programmed cell death protein 1 (PD-1) is a biomarker on the surface of cells with a role in promoting self-tolerance by suppressing the inflammatory activity of T cells. In this work, one peptide of PD-1 was used as the template for molecular imprinting to form magnetic peptide-imprinted poly(ethylene-co-vinyl alcohol) composite nanoparticles (MPIP NPs). The nanoparticles were characterized by dynamic light scattering (DLS), high-performance liquid chromatography (HPLC), Brunauer−Emmett−Teller (BET) analysis, and superconducting quantum interference device (SQUID) analysis. Natural killer 92 (NK-92) cells were added to these composite nanoparticles and then incubated with human hepatoma (HepG2) cells. The viability and the apoptosis pathway of HepG2 were then studied using cell counting kit-8 (CCK8) and quantitative real-time polymerase chain reaction (qRT-PCR), respectively. These nanoparticles were found to significantly enhance the activity of natural killer cells toward HepG2 cells by increasing the expression of nuclear factor kappa B (NF-κB), caspase 8, and especially caspase 3. Programmed cell death protein 1 (PD-1) is a biomarker on the surface of cells with a role in promoting self-tolerance by suppressing the inflammatory activity of T cells. In this work, one peptide of PD-1 was used as the template for molecular imprinting to form magnetic peptide-imprinted poly(ethylene- co -vinyl alcohol) composite nanoparticles (MPIP NPs). The nanoparticles were characterized by dynamic light scattering (DLS), high-performance liquid chromatography (HPLC), Brunauer–Emmett–Teller (BET) analysis, and superconducting quantum interference device (SQUID) analysis. Natural killer 92 (NK-92) cells were added to these composite nanoparticles and then incubated with human hepatoma (HepG2) cells. The viability and the apoptosis pathway of HepG2 were then studied using cell counting kit-8 (CCK8) and quantitative real-time polymerase chain reaction (qRT-PCR), respectively. These nanoparticles were found to significantly enhance the activity of natural killer cells toward HepG2 cells by increasing the expression of nuclear factor kappa B (NF-κB), caspase 8, and especially caspase 3. Programmed cell death protein 1 (PD-1) is a biomarker on the surface of cells with a role in promoting self-tolerance by suppressing the inflammatory activity of T cells. In this work, one peptide of PD-1 was used as the template for molecular imprinting to form magnetic peptide-imprinted poly(ethylene-co-vinyl alcohol) composite nanoparticles (MPIP NPs). The nanoparticles were characterized by dynamic light scattering (DLS), high-performance liquid chromatography (HPLC), Brunauer–Emmett–Teller (BET) analysis, and superconducting quantum interference device (SQUID) analysis. Natural killer 92 (NK-92) cells were added to these composite nanoparticles and then incubated with human hepatoma (HepG2) cells. The viability and the apoptosis pathway of HepG2 were then studied using cell counting kit-8 (CCK8) and quantitative real-time polymerase chain reaction (qRT-PCR), respectively. These nanoparticles were found to significantly enhance the activity of natural killer cells toward HepG2 cells by increasing the expression of nuclear factor kappa B (NF-κB), caspase 8, and especially caspase 3. |
| Author | Liu, Kai-Hsi Chen, Jyun-Ren Thomas, James L. Lin, Hung-Yin Lee, Mei-Hwa |
| AuthorAffiliation | 3 Department of Chemical and Materials Engineering, National University of Kaohsiung, Kaohsiung 81148, Taiwan; 4a140109@stust.edu.tw 1 Department of Materials Science and Engineering, I-Shou University, Kaohsiung 84001, Taiwan; meihwalee@ntu.edu.tw 4 Department of Physics and Astronomy, University of New Mexico, Albuquerque, NM 87131, USA; jthomas@unm.edu 2 Department of Internal Medicine, Division of Cardiology, Zuoying Branch of Kaohsiung Armed Forces General Hospital, Kaohsiung 813, Taiwan; liukaihsi@gmail.com |
| AuthorAffiliation_xml | – name: 3 Department of Chemical and Materials Engineering, National University of Kaohsiung, Kaohsiung 81148, Taiwan; 4a140109@stust.edu.tw – name: 4 Department of Physics and Astronomy, University of New Mexico, Albuquerque, NM 87131, USA; jthomas@unm.edu – name: 1 Department of Materials Science and Engineering, I-Shou University, Kaohsiung 84001, Taiwan; meihwalee@ntu.edu.tw – name: 2 Department of Internal Medicine, Division of Cardiology, Zuoying Branch of Kaohsiung Armed Forces General Hospital, Kaohsiung 813, Taiwan; liukaihsi@gmail.com |
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| Cites_doi | 10.1038/nrgastro.2015.173 10.1038/ni1582 10.1016/j.nantod.2017.10.008 10.1007/s00604-017-2169-4 10.1158/1078-0432.CCR-08-1608 10.1021/ac203422r 10.1056/NEJMoa1504030 10.2217/imt-2017-0022 10.1038/cmi.2015.96 10.1021/am100227r 10.1016/j.seppur.2017.09.071 10.1073/pnas.0712278105 10.1172/JCI66381 10.1186/1756-9966-27-53 10.1016/j.currproblcancer.2017.10.007 10.1016/j.cytogfr.2008.04.001 10.1038/nnano.2007.387 10.1093/nar/29.9.e45 10.5858/arpa.2016-0361-RA 10.1038/bjc.2015.124 10.1039/c2jm34244h 10.1002/j.1460-2075.1992.tb05481.x 10.3389/fimmu.2016.00091 10.1016/j.bios.2006.07.038 10.1039/C5CC09896C 10.4049/jimmunol.1401686 10.1016/j.bios.2009.03.039 10.1016/j.mtchem.2018.01.001 10.1002/j.1460-2075.1995.tb00245.x 10.1038/nri2115 10.1016/j.addr.2017.05.011 10.1093/clinchem/42.9.1506 10.1172/JCI99317 |
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| Keywords | peptide-imprinted polymer natural killer cells human hepatoma cells magnetic nanoparticles programmed cell death protein 1 (PD-1) immunotherapy |
| Language | English |
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| Title | Immunotherapy of Hepatocellular Carcinoma with Magnetic PD-1 Peptide-Imprinted Polymer Nanocomposite and Natural Killer Cells |
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