Deciphering autophagy signaling in cancer: A paradigm shift from molecular classifications to clinical innovations.

Abstract

The intracellular breakdown process known as autophagy occurs when cells experience adverse conditions, such as organelle damage, the presence of abnormal proteins, hypoxia stress, low energy levels, or nutritional deprivation. The autophagic process begins by forming autophagosomes, which then merge with lysosomes to recycle degraded materials. Autophagy functions in multiple ways to affect cancer development and treatment outcomes. Tumor cells with low autophagy levels may exhibit anti-tumor effects during cancer initiation because their connection to malignant transformation is possible. The promotion of autophagy appears beneficial for cancer prevention in this context. The survival of cancer cells through increased autophagy enables tumor growth in existing tumors by allowing them to overcome metabolic and treatment-related challenges. Research indicates that blocking autophagy through the use of drugs or genetic methods makes cancer cells more susceptible to chemotherapy, radiation, and targeted therapies, suggesting that inhibiting the autophagic system may be a promising approach to enhance treatment. Excessive autophagy activation could be a therapeutic approach to manage cancer cells that resist cell death. The successful treatment of cancer requires an understanding of autophagy's dual nature. This review examines potential therapeutic strategies for tumors by analyzing autophagy-related signaling pathways and the essential factors that influence cancer development.