ROS, stress-activated kinases and stress signaling in cancer

Moran Benhar, David Engelberg, Alexander Levitzki*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

549 Scopus citations

Abstract

Anticancer therapy is frequently efficient in early stages of the disease, whereas advanced tumors are usually resistant to the same treatments. The molecular basis for this change is not entirely understood. Many anticancer agents are DNA- or cytoskeleton-damaging drugs that show some specificity towards dividing cells. However, recent studies show that these agents also activate stress-signaling cascades that may play a role in eliciting the observed therapeutic effects. We discuss recent findings that suggest that induction of stress signaling in oncogenically transformed cells is integrated into apoptotic pathways. Reactive oxygen species (ROS) and stress-activated protein kinases (SAPKs), which are potentiated in recently transformed cells, emerge as key effectors of cell death. In advanced tumors, however, these agents are down-regulated and, consequently, death signaling is suppressed. Such changes in ROS and SAPK activity levels during the course of tumor development may underlie the changes in responsiveness to anticancer therapy.

Original languageAmerican English
Pages (from-to)420-425
Number of pages6
JournalEMBO Reports
Volume3
Issue number5
DOIs
StatePublished - 2002

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