Linking ER Stress to Autophagy: Potential Implications for Cancer Therapy
Figure 3
Hypothetic therapeutic strategies based on the modulation of ER stress and autophagy. Different strategies involving modulation of ER stress and autophagy could be potentially used in antitumoral therapies. A. One type of antitumoral agents (e.g., cannabinoids) activates ER stress and autophagy as a mechanism to promote cancer cell death. In these cases, strategies aimed at increasing the stimulation of ER stress and autophagy might be beneficial; B. Other anticancer agents (e.g., PDT) activate ER stress as part of the mechanisms by which they promote cancer cell death. Secondary ER stress-induced activation of autophagy may contribute to cell death (in apoptosis-deficient cells) or to cell survival (in apoptosis competent cells). Thus, depending on the tumor features, autophagy inhibitors or inducers might be administered to improve the response to these anticancer agents. C. A third type of antitumoral agents (e.g., Imatinib mesilate) activates a protective ER stress/autophagy response secondarily to its primary antitumoral mechanism. Inhibition of ER stress and/or autophagy would help to reduce the resistance to this type of therapy.
