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Current Concepts in ER Stress-Induced Apoptosis

Susan E Logue, Adrienne M Gorman, Patricia Cleary, Norma Keogh and Afshin Samali

Tumour development and progression is associated with cancer cell stress, owing to the rapid proliferative rate of cancer cells. During these processes cancer cells encounter severe cytotoxic conditions such as hypoxia, nutrient deprivation, metabolic changes and acidosis. As a consequence cancer cells must possess high adaptive capabilities in order to contend with such stresses. One of the adaptive responses activated in cancer cells is termed the Unfolded Protein Response (UPR), which is triggered by conditions that adversely affect Endoplasmic Reticulum (ER) homeostasis – a condition referred to as ER stress. Activation of the UPR functions to restore ER homeostasis and confer upon cancer cells a survival advantage. If ER stress is prolonged or too severe signalling switches from pro-survival to pro-death and ER stress-induced apoptosis is triggered. In this article we provide an overview of the current concepts concerning ER stress-induced apoptosis, focussing on the role of ER-localized stress sensors and triggering ER stress-induced apoptosis with particular emphasis on the contribution of BCL-2 family members.