Abstract
Autophagy, or self-eating, is a catabolic process that plays a crucial role in cellular homeostasis by carrying out bulk degradation of defective or superfluous proteins as well as worn-out organelles through a specialized structure, the autophagosome, which in turn fuses with the lysosome. Autophagy also alleviates cellular stress induced by nutrient deprivation, metabolic disturbance, hypoxia, and the like, by recycling intracellular constituents. This role of autophagy, to provide metabolic precursors especially upon starvation, might also contribute to the survival of cancer cells. The role of autophagy in cancer cells is ambiguous given that its downregulation or upregulation has been observed to depend on cancer stage and pathological grade. Autophagy has been found to exhibit a dual effect on tumorigenesis where it functions to suppress tumor progression by eliminating factors that cause genome instability while promoting survival of cancer cells under unfavorable conditions like therapeutic stress. This review aims to explain the mechanism, regulation, and the dual role of autophagy in cancer.
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