Title : Differential cytotoxic activity of Quercetin on colonic cancer cells depends on ROS generation through COX-2 expression.

Pub. Date : 2017 Aug

PMID : 28479391






9 Functional Relationships(s)
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1 Differential cytotoxic activity of Quercetin on colonic cancer cells depends on ROS generation through COX-2 expression. Reactive Oxygen Species mitochondrially encoded cytochrome c oxidase II Homo sapiens
2 Increased generation of reactive oxygen species (ROS) was observed only in Quercetin treated HT29 cells, which is due to over expression of COX-2, as COX-2 silencing inhibited Quercetin induced apoptosis and ROS generation. Reactive Oxygen Species mitochondrially encoded cytochrome c oxidase II Homo sapiens
3 Increased generation of reactive oxygen species (ROS) was observed only in Quercetin treated HT29 cells, which is due to over expression of COX-2, as COX-2 silencing inhibited Quercetin induced apoptosis and ROS generation. Reactive Oxygen Species mitochondrially encoded cytochrome c oxidase II Homo sapiens
4 Increased generation of reactive oxygen species (ROS) was observed only in Quercetin treated HT29 cells, which is due to over expression of COX-2, as COX-2 silencing inhibited Quercetin induced apoptosis and ROS generation. Reactive Oxygen Species mitochondrially encoded cytochrome c oxidase II Homo sapiens
5 Increased generation of reactive oxygen species (ROS) was observed only in Quercetin treated HT29 cells, which is due to over expression of COX-2, as COX-2 silencing inhibited Quercetin induced apoptosis and ROS generation. Reactive Oxygen Species mitochondrially encoded cytochrome c oxidase II Homo sapiens
6 Increased generation of reactive oxygen species (ROS) was observed only in Quercetin treated HT29 cells, which is due to over expression of COX-2, as COX-2 silencing inhibited Quercetin induced apoptosis and ROS generation. Reactive Oxygen Species mitochondrially encoded cytochrome c oxidase II Homo sapiens
7 Increased generation of reactive oxygen species (ROS) was observed only in Quercetin treated HT29 cells, which is due to over expression of COX-2, as COX-2 silencing inhibited Quercetin induced apoptosis and ROS generation. Reactive Oxygen Species mitochondrially encoded cytochrome c oxidase II Homo sapiens
8 Insilico analysis provided evidence that Quercetin could partially inhibit COX-2 enzyme by binding to subunit A which has peroxidase activity and serves as source of ROS. Reactive Oxygen Species mitochondrially encoded cytochrome c oxidase II Homo sapiens
9 To conclude, differential sensitivity of two cancer cells, HT29 and HCT15, to Quercetin depends on COX-2 dependent ROS generation that induces apoptosis and inhibits cell survival. Reactive Oxygen Species mitochondrially encoded cytochrome c oxidase II Homo sapiens