Therapeutic potential of autophagy activators and inhibitors in lung and breast cancer- a review

Autophagy is a cellular process that eliminates damaged components of cytoplasm via the lysosome. Autophagy supports cells and tissues to remain healthy by recycling old or damaged cellular organelles and proteins with new ones. The breakdown products that follow are directed into cellular metabolism, where they are utilized to produce energy as well as for maintaining homeostasis and stability of the genome. In many cancers, autophagy modulation carries out a dual role in cancer development and suppression. Autophagy suppresses the proliferation of cancer cells by bringing about cell death and limiting cancer cell development, although it also promotes tumorigenesis by encouraging cancer cell growth and formation. Nevertheless, autophagy's implication in cancer remains a paradox. While several autophagy activators, and inhibitors, such as SAH-EJ2, Gefitinib, Ampelopsin hydroxychloroquine and chloroquine, are utilized to regulate autophagy in chemoprevention, the exact intrinsic system of autophagy in cancer deserves further investigation. Despite improved treatment regimens, the incidence rate of both breast and lung cancer has grown, as has the number of recurrence cases. Hence, this review offers a wide overview of autophagy's underlying role in lung and breast cancer, particularly focusing on the various autophagy activators and inhibitors in both cancers, as well as the use of various organic compounds, regular drugs, and natural products in cancer prevention and treatment.