Autophagy in Cancer Progression and Therapeutics

Autophagy is a catabolic process necessary for maintaining cellular homeostasis. It is triggered by stressors such as nutrient deprivation, hypoxia, DNA damage, or chemotherapy, leading to the formation of autophagosomes that engulf damaged organelles and long-lived proteins. Autophagosomes fuse with lysosomes to form autolysosomes that recycle or remove dysfunctional cargo. Even wild-type or conditionally replicating adenoviruses can trigger autophagy to support infected cell viability for viral DNA delivery and expression of viral proteins, ultimately facilitating oncolysis and viral spread [1,2]. While autophagy helps prevent normal cells from becoming mutated or deregulated, abnormal autophagy is associated with multiple diseases, especially cancer [3]. Autophagy exhibits a controversial dual role: it can promote tumor growth by meeting biosynthetic demands and enabling drug resistance, yet it can suppress early tumorigenesis by clearing damaged organelles and cells [4]. This Special Issue summarizes recent advances in understanding autophagy in cancer progression and therapeutics, including its modulation during chemotherapy and virus-based therapies.

K Kantserova, I Ulasov