Contribution of ER stress to immunogenic cancer cell death

ER stress-induced inflammation is a complex phenomenon which can have either disease-supporting or disease-controlling effects depending on the pathology of the particular disease in focus. In case of cancer it has been observed that ER stress-induced inflammation can have both pro-tumorigenic as well as anti-tumorigenic roles. Thus, therapeutic strategies that can tilt the balance towards anti-tumorigenic role might be our best bet. It has been suggested that therapeutically induced reactive oxygen species (ROS)-based ER stress could instigate within the cancer cells, danger signaling pathways that lead to ‘emission’ of certain damage-associated molecular patterns (DAMPs). These molecules could ultimately cause ‘immunogenic apoptosis,’ a cell death modality that can revive anti-tumor immunity. These new findings point to the importance of therapeutically targeting ER stress-induced inflammation in cancer. In the current chapter we discuss the prospects of inducing ER stress-induced inflammation that supports anti-tumor immunity