ER Stress As Modulator of Autophagy Pathways

Different physiological and pathological situations that produce alterations in the endoplasmic reticulum, lead to a condition known as ER stress homeostasis. ER stress activates a complex intracellular signal transduction pathway, called unfolded protein response (UPR). UPR is tailored essentially to re-establish ER homeostasis. However, when persistent, ER stress can switch the cytoprotective functions of UPR into cell death promoting mechanisms. One of the cellular mechanisms that are regulated by ER stress is autophagy. Autophagy is a cellular process by which different cytoplasmic components including organelles are targeted for degradation to the autophagosomes. Interestingly, like ER stress, autophagy can be a protective or a cell-death promoting mechanism. In this chapter we will review some of the mechanisms that have been proposed to participate in the regulation of autophagy by ER stress and the UPR. Likewise, we will discuss the potential therapeutic implications of the coordinated regulation of these two cellular mechanisms in cancer and cancer treatments.