Mehmet Bostanciklioglu
Programmed cell death plays an important role in development and disease. There are three main types of programmed cell death: apoptosis, autophagy, and necrosis. Apoptosis functions through two basic pathways called extrinsic and intrinsic. When a stressor is present in a cell, apoptosis is initiated. Autophagy is essential for the continuation of normal human physiology such as cell homeostasis, energy balance, development, and cell defense. In addition, it may play a role in the pathogenesis of cancer, neurodegenerative diseases, aging, muscle diseases, infectious diseases, and immune system disorders. While some autophagy genes have shown tumor-suppressive effects during cancer development, other genes contribute to cancer cell survival during cancer progression. Therefore, the relationship between autophagy and cancer is quite complex. The role of autophagy in cancer varies depending on the stage of cancer, metabolic status of the cell, and stress present. In addition, it has been reported that the expression of certain molecules related to autophagy varies in different cancer types. Autophagy is activated and allows continued viability of tumor cells under hypoxia. During nutrient deprivation, autophagy provides time for tumor tissues until nutrients, oxygen, and growth factors become available again. Therefore, autophagy is considered a necessary mechanism for tumor continuity. During cancer treatment, autophagy increases in both cancer cells and normal cells. However, since cancer cells utilize autophagy more than normal cells for survival, this may open new therapeutic opportunities. The studies that need to be conducted to find new ways to utilize the genes involved in autophagy in cancer treatment need to be conducted. In the present study, we aimed to shed light on the interaction of the autophagy mechanism and some stresses such as ischemia and reperfusion and cancer development.