Rigosertib-Activated JNK1/2 Eliminate Tumor Cells through p66Shc Activation.
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ABSTRACT:
SUBMITTER: Gunther JK
PROVIDER: S-EPMC7284707 | biostudies-literature | 2020 May
REPOSITORIES: biostudies-literature
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Rigosertib-Activated JNK1/2 Eliminate Tumor Cells through p66Shc Activation.
Günther Julia K JK Nikolajevic Aleksandar A Ebner Susanne S Troppmair Jakob J Khalid Sana S
Biology 20200515 5
Rigosertib, via reactive oxygen species (ROS), stimulates cJun N-terminal kinases 1/2 (JNK1/2), which inactivate RAS/RAF signaling and thereby inhibit growth and survival of tumor cells. JNK1/2 are not only regulated by ROS-they in turn can also control ROS production. The prooxidant and cell death function of p66Shc requires phosphorylation by JNK1/2. Here, we provide evidence that establishes p66Shc, an oxidoreductase, as a JNK1/2 effector downstream of Rigosertib-induced ROS production, DNA d ...[more]
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