Autophagy, a cellular process that degrades damaged proteins and organelles, plays a dual role in cancer. It acts as both a tumor suppressor by preventing the accumulation of damaged components and as a mechanism for cell survival under stress conditions, promoting tumor growth and therapeutic resistance. In response to hypoxia and increased metabolic demands, tumor cells activate autophagy, which can lead to treatment resistance and tumor dormancy. Preclinical studies have shown that inhibiting autophagy can enhance the efficacy of anti-cancer therapies by restoring chemosensitivity and increasing tumor cell death. Hydroxychloroquine, an autophagy inhibitor, has been tested in early-phase clinical trials, demonstrating its potential as a therapeutic agent. However, more potent and specific autophagy inhibitors are needed to fully exploit this therapeutic target. Understanding the regulation and interplay of autophagy with apoptosis is crucial for optimizing its use in cancer treatment and prevention.Autophagy, a cellular process that degrades damaged proteins and organelles, plays a dual role in cancer. It acts as both a tumor suppressor by preventing the accumulation of damaged components and as a mechanism for cell survival under stress conditions, promoting tumor growth and therapeutic resistance. In response to hypoxia and increased metabolic demands, tumor cells activate autophagy, which can lead to treatment resistance and tumor dormancy. Preclinical studies have shown that inhibiting autophagy can enhance the efficacy of anti-cancer therapies by restoring chemosensitivity and increasing tumor cell death. Hydroxychloroquine, an autophagy inhibitor, has been tested in early-phase clinical trials, demonstrating its potential as a therapeutic agent. However, more potent and specific autophagy inhibitors are needed to fully exploit this therapeutic target. Understanding the regulation and interplay of autophagy with apoptosis is crucial for optimizing its use in cancer treatment and prevention.