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ROS, stress‐activated kinases and stress signaling in cancer
Author(s) -
Benhar Moran,
Engelberg David,
Levitzki Alexander
Publication year - 2002
Publication title -
embo reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.584
H-Index - 184
eISSN - 1469-3178
pISSN - 1469-221X
DOI - 10.1093/embo-reports/kvf094
Subject(s) - signal transduction , microbiology and biotechnology , effector , kinase , reactive oxygen species , programmed cell death , dna damage , apoptosis , cancer cell , biology , cancer research , cancer , chemistry , biochemistry , dna , genetics
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 downregulated 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.