Title : Aspirin Inhibits Natural Killer/T-Cell Lymphoma by Modulation of VEGF Expression and Mitochondrial Function.

Pub. Date : 2018

PMID : 30693272






11 Functional Relationships(s)
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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