Autophagy, a cellular degradation pathway, plays a crucial role in maintaining cellular homeostasis and viability under stress conditions. In tumor cells with defects in apoptosis, autophagy allows prolonged survival. Paradoxically, autophagy defects are associated with increased tumorigenesis, but the underlying mechanisms are not fully understood. Recent evidence suggests that autophagy provides protective functions by limiting tumor necrosis and inflammation, and mitigating genome damage in response to metabolic stress. Autophagy is regulated by the kinase mammalian target of rapamycin (mTOR), which suppresses autophagy in nutrient-rich conditions. In cancer cells, metabolic stress robustly induces autophagy, which is essential for survival. Genetic inactivation of autophagy prevents survival in response to metabolic deprivation, even when apoptosis is blocked. Autophagy-deficient cells fail to tolerate metabolic stress and are defective in the recovery process. Autophagy enables cells to regenerate upon nutrient restoration, demonstrating its resilient capacity for regeneration. In apoptosis-defective tumor cells, autophagy promotes survival through a complex, poorly characterized process. The role of autophagy in tumor dormancy and chemoprevention is also discussed, highlighting its potential as a therapeutic target. The complex interplay between autophagy and cancer, including its integration into metabolism, stress response, and cell-death pathways, is explored, along with future directions for research.Autophagy, a cellular degradation pathway, plays a crucial role in maintaining cellular homeostasis and viability under stress conditions. In tumor cells with defects in apoptosis, autophagy allows prolonged survival. Paradoxically, autophagy defects are associated with increased tumorigenesis, but the underlying mechanisms are not fully understood. Recent evidence suggests that autophagy provides protective functions by limiting tumor necrosis and inflammation, and mitigating genome damage in response to metabolic stress. Autophagy is regulated by the kinase mammalian target of rapamycin (mTOR), which suppresses autophagy in nutrient-rich conditions. In cancer cells, metabolic stress robustly induces autophagy, which is essential for survival. Genetic inactivation of autophagy prevents survival in response to metabolic deprivation, even when apoptosis is blocked. Autophagy-deficient cells fail to tolerate metabolic stress and are defective in the recovery process. Autophagy enables cells to regenerate upon nutrient restoration, demonstrating its resilient capacity for regeneration. In apoptosis-defective tumor cells, autophagy promotes survival through a complex, poorly characterized process. The role of autophagy in tumor dormancy and chemoprevention is also discussed, highlighting its potential as a therapeutic target. The complex interplay between autophagy and cancer, including its integration into metabolism, stress response, and cell-death pathways, is explored, along with future directions for research.