Figure 2 Dominance of the cell-extrinsic effects of autophagy

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Figure 2 Dominance of the cell-extrinsic effects of autophagy Figure 2 | Dominance of the cell-extrinsic effects of autophagy. Functional autophagic responses support the viability of malignant cells in the presence of adverse microenvironmental conditions (including hypoxia, nutrient deprivation and exposure to cytotoxic chemotherapy and/or radiotherapy), hence operating as cell-intrinsic mechanisms of adaptation that favour tumour progression and resistance to treatment. However, autophagy also underlies the capacity of dying cancer cells to release immunostimulatory signals (notably, ATP) and to promote cross-presentation of antigens by dendritic cells (DCs), two processes that are required for the development of therapeutically relevant anticancer immune responses. Moreover, functional autophagic responses are required for immunological competence of the host. Thus, autophagy has a major role as a cell-extrinsic mechanism for the preservation of organismal, over cellular, homeostasis. In immunocompetent hosts, including most patients with cancer, inhibition of autophagy might have a detrimental effect by preventing the development of an antitumor immune response against malignant cells that are resistant to treatment, and might, therefore, result in relapsed disease. Conversely, activation of autophagy might maximize the efficacy of treatments that promote, or at least are compatible with anticancer immunosurveillance, such as radiation therapy. CQ, chloroquine; CRM, caloric-restriction mimetic; HCQ, hydroxychloroquine. Galluzzi, L. et al. (2016) Activating autophagy to potentiate immunogenic chemotherapy and radiation therapy Nat. Rev. Clin. Oncol. doi:10.1038/nrclinonc.2016.183