Autophagy is a cellular process that degrades damaged or unnecessary proteins and organelles, serving as an energy source during metabolic stress. It plays a dual role in cancer: promoting tumor cell survival under stress and, paradoxically, contributing to tumorigenesis when defective. Autophagy helps limit tumor necrosis and inflammation, and mitigates genome damage in response to stress. However, autophagy defects are associated with increased tumorigenesis, though the mechanism remains unclear. Autophagy is regulated by the mTOR pathway, which suppresses autophagy in response to nutrients and growth factors. Starvation or stress triggers autophagy, which is essential for cell survival. In cancer cells, autophagy is induced by metabolic stress and helps sustain survival. However, autophagy defects can lead to necrotic cell death and chronic inflammation, promoting tumor growth. Autophagy also limits genome damage by maintaining protein and organelle quality control, and preventing the accumulation of damaged proteins. Autophagy is involved in both tumor suppression and promotion. Defective autophagy can lead to increased genome damage and tumorigenesis, while autophagy-defective cells are more susceptible to metabolic stress. Autophagy is crucial for maintaining cellular homeostasis and preventing the accumulation of harmful mutations. However, the balance between autophagy's survival and death-promoting roles is complex. Autophagy inhibition can enhance the sensitivity of cancer cells to metabolic stress, leading to necrotic cell death. This process is particularly effective in apoptosis-defective cells. Autophagy inhibitors, such as chloroquine, have shown promise in cancer therapy by promoting necrotic cell death and enhancing the effectiveness of other treatments. Autophagy also plays a role in cancer prevention by managing metabolic stress and reducing genome damage. The role of autophagy in cancer is complex, with both protective and harmful effects. Understanding the mechanisms that regulate autophagy and its interactions with other cellular processes is crucial for developing effective cancer therapies. Future research should focus on the molecular details of autophagy regulation, its role in tumor dormancy, and its potential as a therapeutic target.Autophagy is a cellular process that degrades damaged or unnecessary proteins and organelles, serving as an energy source during metabolic stress. It plays a dual role in cancer: promoting tumor cell survival under stress and, paradoxically, contributing to tumorigenesis when defective. Autophagy helps limit tumor necrosis and inflammation, and mitigates genome damage in response to stress. However, autophagy defects are associated with increased tumorigenesis, though the mechanism remains unclear. Autophagy is regulated by the mTOR pathway, which suppresses autophagy in response to nutrients and growth factors. Starvation or stress triggers autophagy, which is essential for cell survival. In cancer cells, autophagy is induced by metabolic stress and helps sustain survival. However, autophagy defects can lead to necrotic cell death and chronic inflammation, promoting tumor growth. Autophagy also limits genome damage by maintaining protein and organelle quality control, and preventing the accumulation of damaged proteins. Autophagy is involved in both tumor suppression and promotion. Defective autophagy can lead to increased genome damage and tumorigenesis, while autophagy-defective cells are more susceptible to metabolic stress. Autophagy is crucial for maintaining cellular homeostasis and preventing the accumulation of harmful mutations. However, the balance between autophagy's survival and death-promoting roles is complex. Autophagy inhibition can enhance the sensitivity of cancer cells to metabolic stress, leading to necrotic cell death. This process is particularly effective in apoptosis-defective cells. Autophagy inhibitors, such as chloroquine, have shown promise in cancer therapy by promoting necrotic cell death and enhancing the effectiveness of other treatments. Autophagy also plays a role in cancer prevention by managing metabolic stress and reducing genome damage. The role of autophagy in cancer is complex, with both protective and harmful effects. Understanding the mechanisms that regulate autophagy and its interactions with other cellular processes is crucial for developing effective cancer therapies. Future research should focus on the molecular details of autophagy regulation, its role in tumor dormancy, and its potential as a therapeutic target.