Autophagy, a type II programmed cell death, plays a crucial role in cancer through autophagy-related (ATG) proteins. It has dual roles in cancer progression and inhibition, depending on the context and stage of cancer development. In early tumorigenesis, autophagy acts as a survival pathway and quality-control mechanism, preventing tumor initiation and suppressing cancer progression. In late-stage tumors, autophagy supports tumor survival and growth by facilitating metastasis and promoting cancer aggressiveness. Autophagy is involved in various stages of autophagy, including initiation, nucleation, elongation, maturation, fusion, and degradation. Key ATG proteins and complexes, such as the ULK1/2 kinase complex, the class III PI3K complex, the ATG9A trafficking system, and the ATG12 and LC3 ubiquitin-like conjugation systems, are essential for autophagy. Autophagy-related proteins regulate autophagy initiation, nucleation, elongation, maturation, and degradation. Autophagy is involved in maintaining cellular homeostasis, eliminating damaged proteins and organelles, and regulating tumor suppression and promotion. Autophagy can act as a tumor suppressor or promoter, depending on the tumor stage and environment. Autophagy is also involved in cancer therapy, as its regulation can enhance the effectiveness of anticancer treatments. Autophagy plays a dual role in cancer, acting as a tumor suppressor in early stages and a promoter in late stages. Autophagy is essential for cancer cell survival under stress conditions and can contribute to cancer progression and resistance to therapy. Understanding the molecular mechanisms of autophagy and its regulation is crucial for developing effective cancer therapies.Autophagy, a type II programmed cell death, plays a crucial role in cancer through autophagy-related (ATG) proteins. It has dual roles in cancer progression and inhibition, depending on the context and stage of cancer development. In early tumorigenesis, autophagy acts as a survival pathway and quality-control mechanism, preventing tumor initiation and suppressing cancer progression. In late-stage tumors, autophagy supports tumor survival and growth by facilitating metastasis and promoting cancer aggressiveness. Autophagy is involved in various stages of autophagy, including initiation, nucleation, elongation, maturation, fusion, and degradation. Key ATG proteins and complexes, such as the ULK1/2 kinase complex, the class III PI3K complex, the ATG9A trafficking system, and the ATG12 and LC3 ubiquitin-like conjugation systems, are essential for autophagy. Autophagy-related proteins regulate autophagy initiation, nucleation, elongation, maturation, and degradation. Autophagy is involved in maintaining cellular homeostasis, eliminating damaged proteins and organelles, and regulating tumor suppression and promotion. Autophagy can act as a tumor suppressor or promoter, depending on the tumor stage and environment. Autophagy is also involved in cancer therapy, as its regulation can enhance the effectiveness of anticancer treatments. Autophagy plays a dual role in cancer, acting as a tumor suppressor in early stages and a promoter in late stages. Autophagy is essential for cancer cell survival under stress conditions and can contribute to cancer progression and resistance to therapy. Understanding the molecular mechanisms of autophagy and its regulation is crucial for developing effective cancer therapies.