Autophagy is a lysosomal degradation pathway that breaks down intracellular proteins and organelles, playing a critical role in cellular homeostasis and stress response. While autophagy is a tumor-suppressive mechanism, it also enables tumor cells to survive under stress. Autophagy helps maintain cellular metabolism by recycling components during nutrient deprivation and is essential for removing damaged proteins and organelles. Defects in autophagy can lead to cellular dysfunction, increased oxidative stress, and tumor progression. Autophagy is particularly important in tumor cells, which experience high metabolic stress due to hypoxia and nutrient deprivation. Autophagy supports tumor cell survival in hypoxic regions, enabling them to resist therapy and regenerate. However, autophagy defects can impair tumor cell survival and promote tumorigenesis by increasing oxidative stress and inflammation. Autophagy is involved in various aspects of cancer, including tumor suppression and resistance to therapy. Autophagy can promote tumor cell survival by enabling them to withstand metabolic stress and remain dormant. However, autophagy also limits tumorigenesis by clearing damaged proteins and organelles, reducing inflammation, and preventing genome damage. The dual role of autophagy in cancer makes it a complex target for therapy. Autophagy inhibitors can enhance the effectiveness of cancer treatments by blocking tumor cell survival and regeneration, but they may also increase cell death and inflammation. The balance between autophagy's survival and tumor-suppressive functions is crucial for cancer therapy. Autophagy is suppressed in many human tumors, often due to mutations in genes like beclin1 or the PI-3 kinase pathway. These defects can lead to increased tumorigenesis by impairing damage mitigation and promoting chronic inflammation. Autophagy also plays a role in cancer prevention by limiting genome damage and promoting cell death. Strategies to target autophagy in cancer therapy include using autophagy inhibitors to block tumor cell survival and enhance the effectiveness of existing treatments. However, the optimal approach to modulate autophagy for cancer therapy remains a challenge, as the functional status of autophagy varies among tumors. Understanding the role of autophagy in cancer is essential for developing effective therapies that can target both tumor survival and tumor suppression mechanisms.Autophagy is a lysosomal degradation pathway that breaks down intracellular proteins and organelles, playing a critical role in cellular homeostasis and stress response. While autophagy is a tumor-suppressive mechanism, it also enables tumor cells to survive under stress. Autophagy helps maintain cellular metabolism by recycling components during nutrient deprivation and is essential for removing damaged proteins and organelles. Defects in autophagy can lead to cellular dysfunction, increased oxidative stress, and tumor progression. Autophagy is particularly important in tumor cells, which experience high metabolic stress due to hypoxia and nutrient deprivation. Autophagy supports tumor cell survival in hypoxic regions, enabling them to resist therapy and regenerate. However, autophagy defects can impair tumor cell survival and promote tumorigenesis by increasing oxidative stress and inflammation. Autophagy is involved in various aspects of cancer, including tumor suppression and resistance to therapy. Autophagy can promote tumor cell survival by enabling them to withstand metabolic stress and remain dormant. However, autophagy also limits tumorigenesis by clearing damaged proteins and organelles, reducing inflammation, and preventing genome damage. The dual role of autophagy in cancer makes it a complex target for therapy. Autophagy inhibitors can enhance the effectiveness of cancer treatments by blocking tumor cell survival and regeneration, but they may also increase cell death and inflammation. The balance between autophagy's survival and tumor-suppressive functions is crucial for cancer therapy. Autophagy is suppressed in many human tumors, often due to mutations in genes like beclin1 or the PI-3 kinase pathway. These defects can lead to increased tumorigenesis by impairing damage mitigation and promoting chronic inflammation. Autophagy also plays a role in cancer prevention by limiting genome damage and promoting cell death. Strategies to target autophagy in cancer therapy include using autophagy inhibitors to block tumor cell survival and enhance the effectiveness of existing treatments. However, the optimal approach to modulate autophagy for cancer therapy remains a challenge, as the functional status of autophagy varies among tumors. Understanding the role of autophagy in cancer is essential for developing effective therapies that can target both tumor survival and tumor suppression mechanisms.