Autophagy Plays a Dual Role in Drug Resistance

Autophagy is a crucial mechanism that maintains the balance of cellular homeostasis by removing faulty or unneeded proteins as well as damaged or aged organelles in cells. Autophagy is triggered by the formation of autophagosomes, which sequester and enclose anomalous constituents. Subsequently, autophagosomes combine with lysosomes to efficiently recycle or eliminate degradative cargo. Autophagy regulation plays a dual role in both suppressing and promoting cancer in many types of malignancies in a context-dependent manner. In addition, autophagy regulates the characteristics of tumor formation, the spread of cancer, the occurrence of cancer stem cells, and the resistance to drugs used in cancer treatment. Autophagy regulators are employed to modify autophagy for the purpose of anticancer therapy. However, the dual functions of autophagy hinder their effectiveness in this therapy, thereby serving as the primary cause of treatment failure. The chapter provides a concise overview of the mechanisms behind autophagy and its correlation with carcinogenesis, metastasis, and resistance to anticancer drugs. Ultimately, we examine the potential and efficacy of addressing autophagy as a prospective therapeutic approach in anticancer treatment resistance.