Editorial: New roles of autophagy pathways in cancer

Abstract

From a simplistic point of view, autophagy is a self-degradative process that relies on lysosomes for the removal of cytoplasmic bulk cargo and damaged organelles, such as mitochondria. Further on its homeostatic role, autophagy acts as a catabolic process that promotes cellular resilience in conditions of nutrient deprivation and energy depletion. A body of literature has established a crucial role of autophagy in a whole plethora of different physiological processes ranging from homeostasis maintenance, development, and differentiation, among others. In the last two decades, the complexity of autophagy regulation has grown exponentially. Indeed, the literature recognizes canonical and non-canonical autophagic pathways that lead to the degradation and clearance of non-specific or specific cargos (selective autophagy) depending on the cellular context. Due to the fundamental role of autophagy in homeostasis maintenance, it is not surprising its recognized etiologic role in age-related diseases, including cancer. In cancer, autophagy has a dual function, acting as a cell survival mechanism (e.g. favoring the growth of established tumors) or as a tumor suppressor (e.g. preventing the accumulation of damaged proteins and organelles). Thus, the relationship of autophagy with carcinogenesis is complex and, in most cases, it is considered a context-dependent process.