Pub. Date : 2020 Dec 10
PMID : 32560747
14 Functional Relationships(s)Download |
Sentence | Compound Name | Protein Name | Organism |
| 1 | Programmed Death Ligand-1 (PD-L1) regulated by NRF- 2/MicroRNA-1 Regulatory Axis Enhances Drug Resistance and Promotes Tumorigenic Properties in Sorafenib-Resistant Hepatoma Cells. | Sorafenib | CD274 molecule | Homo sapiens |
| 2 | Programmed Death Ligand-1 (PD-L1) regulated by NRF- 2/MicroRNA-1 Regulatory Axis Enhances Drug Resistance and Promotes Tumorigenic Properties in Sorafenib-Resistant Hepatoma Cells. | Sorafenib | CD274 molecule | Homo sapiens |
| 3 | In this study, we reported that PD-L1 wasoverexpressed in sorafenib-resistant hepatoma cells and shRNA-mediated PD-L1depletion attenuated drug-resistance and suppressed the migration, invasion, colonyformation and tumorigenesis in sorafenib-resistant hepatoma cells in vitro and in vivo.Mechanistic investigations indicated that loss of microRNA-1 (miR-1), a tumorsuppressivemicroRNA, contributed to the PD-L1 up-regulation in sorafenib-resistanthepatoma cells and PD-L1 was a direct regulatory target of miR-1. | Sorafenib | CD274 molecule | Homo sapiens |
| 4 | In this study, we reported that PD-L1 wasoverexpressed in sorafenib-resistant hepatoma cells and shRNA-mediated PD-L1depletion attenuated drug-resistance and suppressed the migration, invasion, colonyformation and tumorigenesis in sorafenib-resistant hepatoma cells in vitro and in vivo.Mechanistic investigations indicated that loss of microRNA-1 (miR-1), a tumorsuppressivemicroRNA, contributed to the PD-L1 up-regulation in sorafenib-resistanthepatoma cells and PD-L1 was a direct regulatory target of miR-1. | Sorafenib | CD274 molecule | Homo sapiens |
| 5 | In this study, we reported that PD-L1 wasoverexpressed in sorafenib-resistant hepatoma cells and shRNA-mediated PD-L1depletion attenuated drug-resistance and suppressed the migration, invasion, colonyformation and tumorigenesis in sorafenib-resistant hepatoma cells in vitro and in vivo.Mechanistic investigations indicated that loss of microRNA-1 (miR-1), a tumorsuppressivemicroRNA, contributed to the PD-L1 up-regulation in sorafenib-resistanthepatoma cells and PD-L1 was a direct regulatory target of miR-1. | Sorafenib | CD274 molecule | Homo sapiens |
| 6 | In this study, we reported that PD-L1 wasoverexpressed in sorafenib-resistant hepatoma cells and shRNA-mediated PD-L1depletion attenuated drug-resistance and suppressed the migration, invasion, colonyformation and tumorigenesis in sorafenib-resistant hepatoma cells in vitro and in vivo.Mechanistic investigations indicated that loss of microRNA-1 (miR-1), a tumorsuppressivemicroRNA, contributed to the PD-L1 up-regulation in sorafenib-resistanthepatoma cells and PD-L1 was a direct regulatory target of miR-1. | Sorafenib | CD274 molecule | Homo sapiens |
| 7 | In this study, we reported that PD-L1 wasoverexpressed in sorafenib-resistant hepatoma cells and shRNA-mediated PD-L1depletion attenuated drug-resistance and suppressed the migration, invasion, colonyformation and tumorigenesis in sorafenib-resistant hepatoma cells in vitro and in vivo.Mechanistic investigations indicated that loss of microRNA-1 (miR-1), a tumorsuppressivemicroRNA, contributed to the PD-L1 up-regulation in sorafenib-resistanthepatoma cells and PD-L1 was a direct regulatory target of miR-1. | Sorafenib | CD274 molecule | Homo sapiens |
| 8 | In this study, we reported that PD-L1 wasoverexpressed in sorafenib-resistant hepatoma cells and shRNA-mediated PD-L1depletion attenuated drug-resistance and suppressed the migration, invasion, colonyformation and tumorigenesis in sorafenib-resistant hepatoma cells in vitro and in vivo.Mechanistic investigations indicated that loss of microRNA-1 (miR-1), a tumorsuppressivemicroRNA, contributed to the PD-L1 up-regulation in sorafenib-resistanthepatoma cells and PD-L1 was a direct regulatory target of miR-1. | Sorafenib | CD274 molecule | Homo sapiens |
| 9 | In this study, we reported that PD-L1 wasoverexpressed in sorafenib-resistant hepatoma cells and shRNA-mediated PD-L1depletion attenuated drug-resistance and suppressed the migration, invasion, colonyformation and tumorigenesis in sorafenib-resistant hepatoma cells in vitro and in vivo.Mechanistic investigations indicated that loss of microRNA-1 (miR-1), a tumorsuppressivemicroRNA, contributed to the PD-L1 up-regulation in sorafenib-resistanthepatoma cells and PD-L1 was a direct regulatory target of miR-1. | Sorafenib | CD274 molecule | Homo sapiens |
| 10 | In this study, we reported that PD-L1 wasoverexpressed in sorafenib-resistant hepatoma cells and shRNA-mediated PD-L1depletion attenuated drug-resistance and suppressed the migration, invasion, colonyformation and tumorigenesis in sorafenib-resistant hepatoma cells in vitro and in vivo.Mechanistic investigations indicated that loss of microRNA-1 (miR-1), a tumorsuppressivemicroRNA, contributed to the PD-L1 up-regulation in sorafenib-resistanthepatoma cells and PD-L1 was a direct regulatory target of miR-1. | Sorafenib | CD274 molecule | Homo sapiens |
| 11 | In this study, we reported that PD-L1 wasoverexpressed in sorafenib-resistant hepatoma cells and shRNA-mediated PD-L1depletion attenuated drug-resistance and suppressed the migration, invasion, colonyformation and tumorigenesis in sorafenib-resistant hepatoma cells in vitro and in vivo.Mechanistic investigations indicated that loss of microRNA-1 (miR-1), a tumorsuppressivemicroRNA, contributed to the PD-L1 up-regulation in sorafenib-resistanthepatoma cells and PD-L1 was a direct regulatory target of miR-1. | Sorafenib | CD274 molecule | Homo sapiens |
| 12 | From molecular mechanism insight back to the functional verification,we eventually demonstrated that miR-1 executed its tumor suppressive effects on drugresistanceand other malignant properties in sorafenib-resistant hepatoma cells partiallyby PD-L1 inhibition in vitro and in vivo. | Sorafenib | CD274 molecule | Homo sapiens |
| 13 | In conclusion, our data suggested a NRF-2/miR-1/PD-L1 regulatory axis contributed to development and maintenance of drugCopyright 2020 Cognizant Communication Corporation4ORM-A-3264 Oncology Research E-pubresistance and other tumorigenic properties in sorafenib-resistant hepatoma cells andprovided a potential therapeutic target for overcoming sorafenib resistance in HCC. | Sorafenib | CD274 molecule | Homo sapiens |
| 14 | In conclusion, our data suggested a NRF-2/miR-1/PD-L1 regulatory axis contributed to development and maintenance of drugCopyright 2020 Cognizant Communication Corporation4ORM-A-3264 Oncology Research E-pubresistance and other tumorigenic properties in sorafenib-resistant hepatoma cells andprovided a potential therapeutic target for overcoming sorafenib resistance in HCC. | Sorafenib | CD274 molecule | Homo sapiens |