Pub. Date : 2018
PMID : 30693272
11 Functional Relationships(s)Download |
Sentence | Compound Name | Protein Name | Organism |
1 | Aspirin Inhibits Natural Killer/T-Cell Lymphoma by Modulation of VEGF Expression and Mitochondrial Function. | Aspirin | vascular endothelial growth factor A | Homo sapiens |
2 | In this study, we found that aspirin treatment suppresses VEGF expression in NKTCL SNK-6 cells. | Aspirin | vascular endothelial growth factor A | Homo sapiens |
3 | Further investigation showed that aspirin treatment increases histone methylation in the range of -100~0 that is proximal to the transcription start site on the VEGF promoter, subsequently decreasing the binding ability of Sp1 to the VEGF promoter with VEGF suppression. | Aspirin | vascular endothelial growth factor A | Homo sapiens |
4 | Further investigation showed that aspirin treatment increases histone methylation in the range of -100~0 that is proximal to the transcription start site on the VEGF promoter, subsequently decreasing the binding ability of Sp1 to the VEGF promoter with VEGF suppression. | Aspirin | vascular endothelial growth factor A | Homo sapiens |
5 | Further investigation showed that aspirin treatment increases histone methylation in the range of -100~0 that is proximal to the transcription start site on the VEGF promoter, subsequently decreasing the binding ability of Sp1 to the VEGF promoter with VEGF suppression. | Aspirin | vascular endothelial growth factor A | Homo sapiens |
6 | Aspirin treatment alone slightly inhibits NKTCL SNK-6 tumor growth and EBV replication; while in the presence of histone deacetylase inhibitor (HDACi) chidamide (CDM), aspirin significantly suppresses the VEGF signaling pathway with increased ROS overgeneration and EBV inhibition. | Aspirin | vascular endothelial growth factor A | Homo sapiens |
7 | Aspirin treatment alone slightly inhibits NKTCL SNK-6 tumor growth and EBV replication; while in the presence of histone deacetylase inhibitor (HDACi) chidamide (CDM), aspirin significantly suppresses the VEGF signaling pathway with increased ROS overgeneration and EBV inhibition. | Aspirin | vascular endothelial growth factor A | Homo sapiens |
8 | This is the first time that the potential mechanism for aspirin-mediated VEGF suppression and anti-tumor effect has been discovered, and this study provides a new strategy for anti-tumor drug development for NKTCL treatment based on aspirin-mediated targeting of the VEGF signaling pathway and ROS formation. | Aspirin | vascular endothelial growth factor A | Homo sapiens |
9 | This is the first time that the potential mechanism for aspirin-mediated VEGF suppression and anti-tumor effect has been discovered, and this study provides a new strategy for anti-tumor drug development for NKTCL treatment based on aspirin-mediated targeting of the VEGF signaling pathway and ROS formation. | Aspirin | vascular endothelial growth factor A | Homo sapiens |
10 | This is the first time that the potential mechanism for aspirin-mediated VEGF suppression and anti-tumor effect has been discovered, and this study provides a new strategy for anti-tumor drug development for NKTCL treatment based on aspirin-mediated targeting of the VEGF signaling pathway and ROS formation. | Aspirin | vascular endothelial growth factor A | Homo sapiens |
11 | This is the first time that the potential mechanism for aspirin-mediated VEGF suppression and anti-tumor effect has been discovered, and this study provides a new strategy for anti-tumor drug development for NKTCL treatment based on aspirin-mediated targeting of the VEGF signaling pathway and ROS formation. | Aspirin | vascular endothelial growth factor A | Homo sapiens |