Title : Small-Molecule NSC59984 Induces Mutant p53 Degradation through a ROS-ERK2-MDM2 Axis in Cancer Cells.

Pub. Date : 2022 Apr 1

PMID : 34992144






10 Functional Relationships(s)
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1 Small-molecule NSC59984 induces mutant p53 degradation through a ROS-ERK2-MDM2 axis in cancer cells. Reactive Oxygen Species tumor protein p53 Homo sapiens
2 We used a small-molecule NSC59984 to explore elimination of mutant p53 in cancer cells, and identified an inducible ROS-ERK2-MDM2 axis as a vulnerability for induction of mutant p53 degradation in cancer cells. Reactive Oxygen Species tumor protein p53 Homo sapiens
3 We used a small-molecule NSC59984 to explore elimination of mutant p53 in cancer cells, and identified an inducible ROS-ERK2-MDM2 axis as a vulnerability for induction of mutant p53 degradation in cancer cells. Reactive Oxygen Species tumor protein p53 Homo sapiens
4 High cellular ROS increases the efficacy of NSC59984 targeting mutant p53 degradation and anti-tumor effects. Reactive Oxygen Species tumor protein p53 Homo sapiens
5 Our data suggest that mutant p53 stabilization has a vulnerability under high ROS cellular conditions, which can be exploited by compounds to target mutant p53 protein degradation through the activation of a ROS-ERK2-MDM2 axis in cancer cells. Reactive Oxygen Species tumor protein p53 Homo sapiens
6 Our data suggest that mutant p53 stabilization has a vulnerability under high ROS cellular conditions, which can be exploited by compounds to target mutant p53 protein degradation through the activation of a ROS-ERK2-MDM2 axis in cancer cells. Reactive Oxygen Species tumor protein p53 Homo sapiens
7 Our data suggest that mutant p53 stabilization has a vulnerability under high ROS cellular conditions, which can be exploited by compounds to target mutant p53 protein degradation through the activation of a ROS-ERK2-MDM2 axis in cancer cells. Reactive Oxygen Species tumor protein p53 Homo sapiens
8 Our data suggest that mutant p53 stabilization has a vulnerability under high ROS cellular conditions, which can be exploited by compounds to target mutant p53 protein degradation through the activation of a ROS-ERK2-MDM2 axis in cancer cells. Reactive Oxygen Species tumor protein p53 Homo sapiens
9 Implications: An inducible ROS-ERK2-MDM2 axis exposes a vulnerability in mutant p53 stabilization and can be exploited by small molecule compounds to induce mutant p53 degradation for cancer therapy. Reactive Oxygen Species tumor protein p53 Homo sapiens
10 Implications: An inducible ROS-ERK2-MDM2 axis exposes a vulnerability in mutant p53 stabilization and can be exploited by small molecule compounds to induce mutant p53 degradation for cancer therapy. Reactive Oxygen Species tumor protein p53 Homo sapiens