Autophagy is a genetic program that secures the survival of eukaryotic cells to compensate for periods of starvation and cellular stress. Apoptosis, in contrast, is a genetically defined program leading to cell death. Both pathways are interconnected through conserved co-regulatory signaling pathways that are context-dependent. Proper co-regulation of autophagy and apoptosis, whereby autophagy exerts an antiapoptotic function and apoptosis inhibits autophagic survival strategies, critically secures the survival of healthy cells and counteracts genomic instability in eukaryotic organisms. Cancer cells often become resistant to apoptosis and addicted to autophagy, making this scenario highly relevant to define novel therapeutic strategies. The co-regulatory crosstalk between apoptosis and autophagy converges on the production of phosphatidylinositol 3-phosphate (PI3P) essential for the onset of autophagy. WD-repeat protein interacting with phosphoinositides (WIPI) members function as essential PI3P effectors in autophagy and fulfill an important role in health and disease. Here, we summarize details on the regulation of WIPI-mediated autophagy in the context of co-regulatory signals for both apoptosis and autophagy.
Part of the book: Cell Death