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The growth of cancer cells is limited by energy supply which is regulatedby the energy sensor AMP-kinase (AMPK). Hence, mimicking a low energy state mayinhibit cancer growth and may be exploited in anticancer therapies. In the presentstudy, the impact of AMPK activation on cell growth and apoptosis of DU-145 prostatecancer cells was investigated. Incubation with the AMPK activator aminoimidazolecarboxamide ribonucleotide (AICAR) dose-dependently inhibited cell growth, activatedAMPK, and inhibited mTOR. Furthermore, AICAR treatment activated c-Jun N-terminalkinase (JNK) and caspase-3, thereby initiating apoptosis. Within 60 min of treatmentAICAR raised intracellular reactive oxygen species (ROS) which could be abolishedin the presence of the free radical scavenger N-(2-mercaptopropionyl)glycin (NMPG),the AMPK inhibitor compound C (Comp C) and the respiratory chain complex I inhibitorrotenone, but not by the NADPH oxidase inhibitor VAS2870. Inhibition of ROS generationabolished AMPK activation by AICAR as well as JNK and caspase-3 activation. Furthermore,AMPK activation, JNK phosphorylation and cleaved caspase-3 upon AICAR treatmentwere abolished in the presence of Comp C. In summary, our data demonstrate thatactivation of AMPK by AICAR induces apoptosis of prostate cancer cells by a signalingpathway involving ROS, activation of JNK and cleaved caspase-3.

international journal of oncology

Activation of AMP-kinase by AICAR induces apoptosis of DU-145 prostate cancer cells through generation of reactive oxygen species and activation of c-Jun N-terminal kinase