Roles for the Stress-Responsive Kinases ASK1 and ASK2 in Tumorigenesis

Eukaryotic cells sense a wide range of biological and physicochemical stressors from both external and internal environments and convert them to physiological signals that lead to appropriate responses. Some stressors cause cellular damage, resulting in the activation of the cellular repair mechanism. In cases of severe damage, cells undergo apoptosis, which prevents uncontrollable cell proliferation. Stress-responsive signaling pathways elaborately regulate this defense mechanism against cytotoxic stressors, and their dysfunction can lead to tumorigenesis. Most of these pathways are also activated during inflammatory responses that, while intrinsically host defensive, increase the risk of tumorigenesis, especially when the response is chronic. Therefore, the stress-responsive signaling pathways that regulate apoptosis and inflammation are important as research subjects to explore the mechanisms of tumorigenesis and as therapeutic targets of cancer.