Autophagy, a cellular process that degrades and recycles intracellular components, plays a dual role in cancer. It can suppress cancer by eliminating oncogenic proteins, damaged organelles, and toxic unfolded proteins, or promote cancer by supporting metabolic needs and mitochondrial function in established tumors. The context-specific role of autophagy in cancer is crucial for therapeutic strategies. Autophagy is essential for maintaining cellular homeostasis, especially under stress or starvation, by recycling materials and maintaining mitochondrial quality. Defects in autophagy lead to the accumulation of damaged proteins and organelles, increasing oxidative stress and promoting cancer development. Autophagy also influences antioxidant defense through the regulation of NRF2, a key transcription factor involved in stress response. Autophagy defects can lead to the accumulation of p62, which disrupts signaling pathways and promotes tumorigenesis. Conversely, autophagy can support cancer cell survival during stress, particularly in hypoxic environments, and is required for mitochondrial function and energy metabolism. Autophagy is also involved in tumor suppression by maintaining mitochondrial quality and preventing genomic instability. In some cancers, autophagy is essential for survival, and its inhibition can lead to tumor cell death. However, autophagy can also be exploited by cancer cells to survive under metabolic stress. The role of autophagy in cancer is complex, with both tumor-suppressive and tumor-promoting functions depending on the cellular context. Understanding the mechanisms of autophagy in cancer is essential for developing effective therapies. Autophagy inhibition may enhance the effectiveness of cancer treatments by increasing cellular stress and promoting tumor cell death. However, the use of autophagy inhibitors must be carefully evaluated to avoid unintended side effects. Overall, autophagy is a critical process in cancer biology, with implications for both cancer prevention and treatment.Autophagy, a cellular process that degrades and recycles intracellular components, plays a dual role in cancer. It can suppress cancer by eliminating oncogenic proteins, damaged organelles, and toxic unfolded proteins, or promote cancer by supporting metabolic needs and mitochondrial function in established tumors. The context-specific role of autophagy in cancer is crucial for therapeutic strategies. Autophagy is essential for maintaining cellular homeostasis, especially under stress or starvation, by recycling materials and maintaining mitochondrial quality. Defects in autophagy lead to the accumulation of damaged proteins and organelles, increasing oxidative stress and promoting cancer development. Autophagy also influences antioxidant defense through the regulation of NRF2, a key transcription factor involved in stress response. Autophagy defects can lead to the accumulation of p62, which disrupts signaling pathways and promotes tumorigenesis. Conversely, autophagy can support cancer cell survival during stress, particularly in hypoxic environments, and is required for mitochondrial function and energy metabolism. Autophagy is also involved in tumor suppression by maintaining mitochondrial quality and preventing genomic instability. In some cancers, autophagy is essential for survival, and its inhibition can lead to tumor cell death. However, autophagy can also be exploited by cancer cells to survive under metabolic stress. The role of autophagy in cancer is complex, with both tumor-suppressive and tumor-promoting functions depending on the cellular context. Understanding the mechanisms of autophagy in cancer is essential for developing effective therapies. Autophagy inhibition may enhance the effectiveness of cancer treatments by increasing cellular stress and promoting tumor cell death. However, the use of autophagy inhibitors must be carefully evaluated to avoid unintended side effects. Overall, autophagy is a critical process in cancer biology, with implications for both cancer prevention and treatment.