Autophagy modulation in gynaecologic oncology: insights into immune regulation and therapeutic potential

As a fundamental cellular process, autophagy maintains homeostasis and viability through the regulation of proteostasis, organelle quality control, and functional preservation. It represents the central pathway for transporting diverse cytoplasmic components to lysosomes for degradation and recycling. Accumulating evidence reveals the paradoxical role of autophagy in oncogenesis, where it can either suppress tumour development or facilitate cancer progression depending on context and stage. This conclusion is particularly evident during gynaecological tumour progression. Contemporary research priorities include deciphering the intricate involvement of autophagy in antitumour immunity and treatment resistance mechanisms. This comprehensive analysis systematically evaluates the dichotomous nature of autophagic processes across various malignancies and developmental phases, with a particular emphasis on how autophagy influences the dynamics of the gynaecological tumour microenvironment and modulates treatment responses. Key findings reveal that autophagy regulates immune checkpoint expression (e.g., PD-L1 and MHC-I); shapes antitumour immunity via T cells, macrophages, and other immune components; and modulates drug resistance through pathways involving AMP-activated protein kinase (AMPK), Heat shock factor 1 (HSF1), and Reactive oxygen species (ROS). These findings underscore the potential of autophagy as a therapeutic target and highlight strategies for combining autophagy modulators with conventional treatments to overcome resistance. This article provides a foundation for the development of precision medicine approaches tailored to autophagy-related pathways in gynaecologic malignancies.