Role of Autophagy and Oxidative Stress in Cancer Metastasis

Autophagy serves as a vital mechanism for cellular repair, to isolate misfolded proteins, dysfunctional proteins, and damaged cell organelles. The malfunctioning autophagy process has been associated with various diseases, including infectious and neurodegenerative diseases, type 2 diabetes mellitus, and cancer. Organisms constantly face oxidative stress to some extent, primarily due to reactive oxygen and nitrogen species. Research has demonstrated that autophagy is readily triggered by reactive oxygen species (ROS) in the absence of nutrients. In recent times, there has been an increasing focus on identifying new therapeutic targets related to the autophagy process. Autophagy is induced during the progression of different human cancers toward metastasis. Through the use of genetically engineered mice and experimental metastasis models, the involvement of autophagy in nearly every stage of the metastatic process has been identified. More specifically, autophagy has been found to play a role in regulating tumor cell motility and invasion, the viability and differentiation of cancer stem cells, resistance to anoikis, the transition from epithelial to mesenchymal state, tumor cell dormancy, escape from immune surveillance, and also in the establishment of the pre-metastatic niche and other aspects of metastasis. In this literature review, our aim is to provide an overview of the connection between autophagy, oxidative stress, and carcinogenesis.