Abstract
Autophagy is an intracellular degradative process that occurs under several stressful conditions, including organelle damage, the presence of abnormal proteins, and nutrient deprivation. The mechanism of autophagy initiates the formation of autophagosomes that capture degraded components and then fuse with lysosomes to recycle these components. The modulation of autophagy plays dual roles in tumor suppression and promotion in many cancers. In addition, autophagy regulates the properties of cancer stem-cells by contributing to the maintenance of stemness, the induction of recurrence, and the development of resistance to anticancer reagents. Although some autophagy modulators, such as rapamycin and chloroquine, are used to regulate autophagy in anticancer therapy, since this process also plays roles in both tumor suppression and promotion, the precise mechanism of autophagy in cancer requires further study. In this review, we will summarize the mechanism of autophagy under stressful conditions and its roles in tumor suppression and promotion in cancer and in cancer stem-cells. Furthermore, we discuss how autophagy is a promising potential therapeutic target in cancer treatment.
Highlights
Autophagy is a physiological cellular process for the degradation and elimination of misfolded proteins and damaged organelles that functions in adaptation to starvation, development, cell death, and tumor suppression [1,2]
Autophagy is regulated by complex intracellular processes under stressful conditions, including nutrient deprivation, the presence of damaged organelles, and anticancer therapy
Many studies have found that autophagy plays dual roles in cell survival and cell death in the context of tumor initiation and development
Summary
Autophagy is a physiological cellular process for the degradation and elimination of misfolded proteins and damaged organelles that functions in adaptation to starvation, development, cell death, and tumor suppression [1,2]. One of the important mechanisms of autophagy is an intracellular degradation pathway mediated by double membrane vesicles called autophagosomes. These autophagosomes deliver degraded cytoplasmic components to the lysosome to be recycled during stressful conditions. This mechanism of autophagy is essential for protecting cells from damaged proteins, to shield cell organelles from toxins, to maintain cell metabolism and energy homeostasis, and to promote cell survival (Figure 1). We discuss autophagy as a therapeutic target in cancer treatment
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